Raras
Buscar doenças, sintomas, genes...
Doença do transporte membranar mitocondrial
ORPHA:254827CID-11 · 5C53.3DOENÇA RARA

Leite é uma secreção nutritiva de cor esbranquiçada e opaca produzida pelas glândulas mamárias das fêmeas dos mamíferos.

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Introdução

O que você precisa saber de cara

📋

Doença rara do transporte membranar mitocondrial, caracterizada por hepatoesplenomegalia, distrofia corneana e déficit de crescimento. Apresenta morfologia mitocondrial anormal, desconforto respiratório e insuficiência cardíaca congestiva de baixo débito.

Publicações científicas
31 artigos
Último publicado: 2026 Jan
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SUS: Sem cobertura SUSScore: 0%
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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

🧠
Neurológico
19 sintomas
💪
Músculos
9 sintomas
👁️
Olhos
8 sintomas
🫃
Digestivo
7 sintomas
❤️
Coração
6 sintomas
🫁
Pulmão
5 sintomas

+ 39 sintomas em outras categorias

Características mais comuns

Hepatoesplenomegalia
Distrofia corneana
Eletroretinograma anormal
Déficit de crescimento
Morfologia anormal da mitocôndria
Desconforto respiratório
107sintomas
Sem dados (107)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 107 características clínicas mais associadas, ordenadas por frequência.

HepatoesplenomegaliaHepatosplenomegaly
Distrofia corneanaCorneal dystrophy
Eletroretinograma anormalAbnormal electroretinogram
Déficit de crescimentoFailure to thrive
Morfologia anormal da mitocôndriaAbnormality of the mitochondrion

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1
Total histórico31PubMed
Últimos 10 anos200publicações
Pico2026115 papers
Linha do tempo
2025Hoje · 2026🧪 2009Primeiro ensaio clínico
Publicações por ano (últimos 10 anos)

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Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

7 genes identificados com associação a esta condição.

SLC25A3Solute carrier family 25 member 3Disease-causing germline mutation(s) inRestrito
FUNÇÃO

Inorganic ion transporter that transports phosphate or copper ions across the mitochondrial inner membrane into the matrix compartment (By similarity) (PubMed:17273968, PubMed:29237729). Mediates proton-coupled symport of phosphate ions necessary for mitochondrial oxidative phosphorylation of ADP to ATP (By similarity) (PubMed:17273968). Transports copper ions probably in the form of anionic copper(I) complexes to maintain mitochondrial matrix copper pool and to supply copper for cytochrome C ox

LOCALIZAÇÃO

Mitochondrion inner membrane

VIAS BIOLÓGICAS (1)
Mitochondrial iron-sulfur cluster biogenesis
MECANISMO DE DOENÇA

Mitochondrial phosphate carrier deficiency

An autosomal recessive disorder of oxidative phosphorylation. Patients have lactic acidosis, hypertrophic cardiomyopathy and muscular hypotonia and die within the first year of life.

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
211.3 TPM
Coração - Ventrículo esquerdo
192.9 TPM
Linfócitos
171.1 TPM
Músculo esquelético
169.3 TPM
Glândula adrenal
164.3 TPM
OUTRAS DOENÇAS (1)
cardiomyopathy-hypotonia-lactic acidosis syndrome
HGNC:10989UniProt:Q00325
TKFCTriokinase/FMN cyclaseCandidate gene tested inTolerante
FUNÇÃO

Catalyzes both the phosphorylation of dihydroxyacetone and of glyceraldehyde, and the splitting of ribonucleoside diphosphate-X compounds among which FAD is the best substrate. Represses IFIH1-mediated cellular antiviral response (PubMed:17600090)

LOCALIZAÇÃO

VIAS BIOLÓGICAS (4)
DDX58/IFIH1-mediated induction of interferon-alpha/betaSARS-CoV-2 activates/modulates innate and adaptive immune responsesSARS-CoV-1 activates/modulates innate immune responsesFructose catabolism
MECANISMO DE DOENÇA

Triokinase and FMN cyclase deficiency syndrome

An autosomal recessive disease characterized by cataracts and developmental delay that may be associated with cerebellar hypoplasia. Additional features may include liver dysfunction, microcytic anemia, and fatal cardiomyopathy with lactic acidosis following a febrile illness.

EXPRESSÃO TECIDUAL(Ubíquo)
Glândula adrenal
87.4 TPM
Intestino delgado
50.0 TPM
Testículo
43.6 TPM
Fígado
40.1 TPM
Linfócitos
29.6 TPM
OUTRAS DOENÇAS (2)
triokinase and FMN cyclase deficiency syndromeSengers syndrome
HGNC:24552UniProt:Q3LXA3
SLC25A4ADP/ATP translocase 1Candidate gene tested inModerado
FUNÇÃO

ADP:ATP antiporter that mediates import of ADP into the mitochondrial matrix for ATP synthesis, and export of ATP out to fuel the cell (PubMed:21586654, PubMed:27693233, PubMed:23173940, PubMed:30046662). Cycles between the cytoplasmic-open state (c-state) and the matrix-open state (m-state): operates by the alternating access mechanism with a single substrate-binding site intermittently exposed to either the cytosolic (c-state) or matrix (m-state) side of the inner mitochondrial membrane (By si

LOCALIZAÇÃO

Mitochondrion inner membraneMembrane

VIAS BIOLÓGICAS (1)
Mitochondrial protein import
MECANISMO DE DOENÇA

Progressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal dominant, 2

A disorder characterized by progressive weakness of ocular muscles and levator muscle of the upper eyelid. In a minority of cases, it is associated with skeletal myopathy, which predominantly involves axial or proximal muscles and which causes abnormal fatigability and even permanent muscle weakness. Ragged-red fibers and atrophy are found on muscle biopsy. A large proportion of chronic ophthalmoplegias are associated with other symptoms, leading to a multisystemic pattern of this disease. Additional symptoms are variable, and may include cataracts, hearing loss, sensory axonal neuropathy, ataxia, depression, hypogonadism, and parkinsonism.

EXPRESSÃO TECIDUAL(Ubíquo)
Coração - Ventrículo esquerdo
563.9 TPM
Coração - Átrio
428.0 TPM
Músculo esquelético
370.5 TPM
Cérebro - Hemisfério cerebelar
138.9 TPM
Esôfago - Muscular
110.1 TPM
OUTRAS DOENÇAS (5)
mitochondrial DNA depletion syndrome 12B (cardiomyopathic type), autosomal recessivemitochondrial DNA depletion syndrome 12A (cardiomyopathic type), autosomal dominantprogressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal dominant 2autosomal dominant progressive external ophthalmoplegia
HGNC:10990UniProt:P12235
AGKAcylglycerol kinase, mitochondrialDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Lipid kinase that can phosphorylate both monoacylglycerol and diacylglycerol to form lysophosphatidic acid (LPA) and phosphatidic acid (PA), respectively (PubMed:15939762). Does not phosphorylate sphingosine (PubMed:15939762). Phosphorylates ceramide (By similarity). Phosphorylates 1,2-dioleoylglycerol more rapidly than 2,3-dioleoylglycerol (By similarity). Independently of its lipid kinase activity, acts as a component of the TIM22 complex (PubMed:28712724, PubMed:28712726). The TIM22 complex m

LOCALIZAÇÃO

Mitochondrion inner membraneMitochondrion intermembrane space

VIAS BIOLÓGICAS (1)
Glycerophospholipid biosynthesis
MECANISMO DE DOENÇA

Mitochondrial DNA depletion syndrome 10

An autosomal recessive mitochondrial disorder characterized by congenital cataracts, hypertrophic cardiomyopathy, skeletal myopathy, exercise intolerance, and lactic acidosis. Mental development is normal, but affected individuals may die early from cardiomyopathy.

OUTRAS DOENÇAS (3)
cataract 38Sengers syndrometotal early-onset cataract
HGNC:21869UniProt:Q53H12
GLRX5Glutaredoxin-related protein 5, mitochondrialDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Monothiol glutaredoxin involved in mitochondrial iron-sulfur (Fe/S) cluster transfer (PubMed:20364084, PubMed:23615440). Receives 2Fe/2S clusters from scaffold protein ISCU and mediates their transfer to apoproteins, to the 4Fe/FS cluster biosynthesis machinery, or export from mitochondrion (PubMed:20364084, PubMed:23615440, PubMed:24334290). Required for normal regulation of hemoglobin synthesis by the iron-sulfur protein ACO1 (PubMed:20364084)

LOCALIZAÇÃO

Mitochondrion matrix

VIAS BIOLÓGICAS (1)
Mitochondrial iron-sulfur cluster biogenesis
MECANISMO DE DOENÇA

Anemia, sideroblastic, 3, pyridoxine-refractory

A form of sideroblastic anemia, a bone marrow disorder defined by the presence of pathologic iron deposits in erythroblast mitochondria. Sideroblastic anemia is characterized by anemia of varying severity, hypochromic peripheral erythrocytes, systemic iron overload secondary to chronic ineffective erythropoiesis, and the presence of bone marrow ringed sideroblasts. Sideroblasts are characterized by iron-loaded mitochondria clustered around the nucleus. SIDBA3 is refractory to treatment with vitamin B6, while iron chelation therapy may result in clinical improvement. SIDBA3 inheritance is autosomal recessive.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
65.0 TPM
Glândula adrenal
55.8 TPM
Músculo esquelético
48.2 TPM
Ovário
43.3 TPM
Rim - Medula
42.5 TPM
OUTRAS DOENÇAS (2)
spasticity-ataxia-gait anomalies syndromesideroblastic anemia 3
HGNC:20134UniProt:Q86SX6
SLC25A26Mitochondrial S-adenosylmethionine carrier proteinDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Mitochondrial S-adenosyl-L-methionine/S-adenosyl-L-homocysteine antiporter. Mediates the exchange of cytosolic S-adenosyl-L-methionine, the predominant methyl-group donor for macromolecule methylation processes, for mitochondrial S-adenosylhomocysteine(SAH), a by-product of methylation reactions

LOCALIZAÇÃO

Mitochondrion inner membrane

VIAS BIOLÓGICAS (1)
SLC-mediated transport of organic cations
MECANISMO DE DOENÇA

Combined oxidative phosphorylation deficiency 28

An autosomal recessive mitochondrial disorder characterized by decreased activities of respiratory chain enzymes, and variable clinical manifestations. Clinical features include episodic metabolic decompensation beginning in infancy, mild muscle weakness, cardiorespiratory insufficiency, developmental delay, or even death.

EXPRESSÃO TECIDUAL(Ubíquo)
Tireoide
12.1 TPM
Ovário
12.1 TPM
Artéria tibial
12.0 TPM
Skin Sun Exposed Lower leg
12.0 TPM
Cólon sigmoide
11.8 TPM
INTERAÇÕES PROTEICAS (3)
OUTRAS DOENÇAS (1)
combined oxidative phosphorylation deficiency 28
HGNC:20661UniProt:Q70HW3
SLC25A12Electrogenic aspartate/glutamate antiporter SLC25A12, mitochondrialDisease-causing germline mutation(s) inRestrito
FUNÇÃO

Mitochondrial electrogenic aspartate/glutamate antiporter that favors efflux of aspartate and entry of glutamate and proton within the mitochondria as part of the malate-aspartate shuttle (PubMed:11566871, PubMed:19641205, PubMed:24515575, PubMed:38945283). Also mediates the uptake of L-cysteinesulfinate (3-sulfino-L-alanine) by mitochondria in exchange of L-glutamate and proton (PubMed:11566871). Can also exchange L-cysteinesulfinate with aspartate in their anionic form without any proton trans

LOCALIZAÇÃO

Mitochondrion inner membrane

VIAS BIOLÓGICAS (2)
Aspartate and asparagine metabolismMalate-aspartate shuttle
MECANISMO DE DOENÇA

Developmental and epileptic encephalopathy 39 with leukodystrophy

A form of epileptic encephalopathy, a heterogeneous group of severe early-onset epilepsies characterized by refractory seizures, neurodevelopmental impairment, and poor prognosis. Development is normal prior to seizure onset, after which cognitive and motor delays become apparent. DEE39 is characterized by global hypomyelination of the central nervous system, with the gray matter appearing relatively unaffected. Inheritance is autosomal recessive.

EXPRESSÃO TECIDUAL(Ubíquo)
Músculo esquelético
70.2 TPM
Cérebro - Hemisfério cerebelar
57.9 TPM
Esôfago - Muscular
47.6 TPM
Cerebelo
46.4 TPM
Brain Frontal Cortex BA9
46.4 TPM
OUTRAS DOENÇAS (1)
developmental and epileptic encephalopathy, 39
HGNC:10982UniProt:O75746

Variantes genéticas (ClinVar)

195 variantes patogênicas registradas no ClinVar.

🧬 SLC25A3: NM_002635.4(SLC25A3):c.562C>T (p.Arg188Ter) ()
🧬 SLC25A3: NM_005888.4(SLC25A3):c.158-1_164del ()
🧬 SLC25A3: NM_002635.4(SLC25A3):c.5_14del (p.Phe2fs) ()
🧬 SLC25A3: NM_002635.4(SLC25A3):c.358A>G (p.Lys120Glu) ()
🧬 SLC25A3: NC_000012.11:g.(?_98987757)_(98989355_?)del ()
Ver todas no ClinVar

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Publicações mais relevantes

Timeline de publicações
0 papers (10 anos)
#1

Mitochondrial Iron Handling and Lipid Peroxidation as Drivers of Ferroptosis.

International journal of molecular sciences2026 Feb 27

Mitochondria are a key organelle in maintaining metabolic homeostasis. It not only generates most of the cell's energy through oxidative phosphorylation but also acts as a complex sensor of the redox state and oxygen in the cell. This review thoroughly analyzes the interactions among mitochondrial iron metabolism, mitochondrial reactive oxygen species (mtROS), and lipid peroxidation (LPO), the triggering factors of ferroptosis, an iron-dependent form of programmed cell death. We point out research showing that intrinsic mitochondrial machinery, such as iron-sulfur (Fe-S) cluster assembly and heme metabolism, is both an important cofactor and a master regulator. If these processes are disrupted, they can lead to ferroptosis. Unlike views that focus on the cytosol, we explain that the stability of Fe-S clusters in complexes such as aconitase and respiratory Complex I is crucial for preventing electron leakage and excessive mtROS formation. The Fenton reaction and its direct effect on cardiolipin (CL) oxidation in the inner membrane of mitochondria is a central event in cardiometabolic diseases. Its peroxidation and breakdown make the organelle very unstable and lead to cell death though Ca2+ overload and a significantly decreased reduced/oxidized glutathione ratio. Additionally, the functions of essential iron transporters and glutathione homeostasis are examined, and their dysregulation is correlated with ferroptosis-associated progression of cardiometabolic and neurodegenerative disorders, such as obesity and Alzheimer's disease. This review focused on the need to revisit the classic bioenergetic core of the mitochondria as a key player in the pathophysiology of metabolic and neurodegenerative diseases.

#2

The genetic architecture of postoperative delirium after major surgery and its relationship with nonpostoperative neurocognitive conditions: A genome-wide association study.

PLoS medicine2026 Mar

Postoperative delirium is the most common postoperative complication in older individuals. Genome-wide association studies (GWAS) can provide insights into how genetic factors influence postoperative risk. We examined the genetic architecture of postoperative delirium after major surgery and its relationship with related cognitive conditions (delirium of any type and Alzheimer's disease, including the APOE ε4 allele). A case-control GWAS was performed in the UK Biobank to identify genetic variants associated with postoperative delirium, adjusted for age, sex, genetic chip, and the first 10 principal components. These results were then used in genetic correlation and polygenic risk score analyses to investigate shared genetic risk between postoperative delirium and a) delirium of all causes, and b) Alzheimer's disease. The GWAS (1,016 cases, 139,148 controls) identified seven Single Nucleotide Polymorphisms (SNPs) that mapped to four genes (APOE, TOMM40, APOC1, and PVRL2); p < 5 x 10-8. Five SNPs remained significant after excluding pre-existing dementia, and two after excluding subsequent dementia. The lead SNP was rs429358, a missense variant of APOE. Genetic correlation and polygenic risk score analyses revealed evidence of shared genetic architecture and risk between postoperative delirium and Alzheimer's disease (rho 0.68, 95% CI [0.46, 0.81]; p < 0.001). After adjustment for age and sex, the APOE ε4 isoform had a dose-response effect on risk (odds ratios for one and two copies: 1.75, 95% CI [1.53, 2.0], and 4.19, 95% CI [3.25, 5.41], respectively; p < 0.001). The main limitations of the study include the reliance upon clinical coding for outcome definition and limited statistical power to detect small or modest genetic effects. We identified genetic variants associated with increased risk of postoperative delirium. We also found evidence of shared genetic liability with Alzheimer's disease via APOE, complementing recent large-scale studies in all-cause delirium. If validated, the findings have potential clinical applications, including preoperative risk stratification and early identification of pre-clinical Alzheimer's disease risk.

#3

ITPR2 Promotes Acute Myeloid Leukemia Progression Through Calcium-Mediated Mitochondrial Dysfunction.

Frontiers in bioscience (Landmark edition)2026 Feb 13

Acute myeloid leukemia (AML) is a hematological malignancy of the myeloid lineage with poor clinical outcomes due to limited targeted therapies. This study elucidates the role of inositol 1,4,5-trisphosphate receptor type 2 (ITPR2) in regulating cell apoptosis by modulating mitochondrial calcium (Ca2+) levels and underscores the clinical significance of ITPR2. ITPR2 expression in patients with AML compared with that of healthy controls using the quantitative real-time PCR (RT-qPCR) method. The role of ITPR2 in AML and its association with immune infiltration levels were investigated through bioinformatics analyses. ITPR2 knockdown in Tohoku Hospital Pediatrics-1 (THP-1) cells were achieved using small interfering RNA (siRNA) and 2-aminoethyl diphenylborinate (2-APB), followed by comprehensive molecular characterization employing RT-qPCR, western blotting (WB), cell counting kit-8 (CCK-8) assays, and flow cytometry. ITPR2 was validated as being highly expressed in patients with AML, and this expression correlated with risk stratification and poor prognosis. Functional enrichment analysis revealed that ITPR2 is involved in Ca2+ signaling pathways and mitochondrial-related biological processes, and its expression level was negatively correlated with immune infiltration levels. Knockdown of ITPR2 or inhibition of its activity with 2-APB reduced Ca2+ ion concentrations in both the cytoplasm and mitochondria, leading to mitochondrial dysfunction (characterized by elevated intracellular reactive oxygen species (ROS) levels, reduced mitochondrial membrane potential (MMP) levels, and reduced mitochondrial DNA copy number) and eventually AML cell apoptosis. ITPR2 facilitates AML progression via the Ca2+-mitochondrial axis and may serve as a prognostic factor and potential therapeutic target.

#4

A Novel PPARG R212W Variant Causes Familial Partial Lipodystrophy Type 3: Clinical Presentation and Functional Characterization.

International journal of molecular sciences2026 Feb 14

Familial partial lipodystrophy type 3 (FPLD3) is a rare autosomal dominant disorder caused by mutations in peroxisome proliferator-activated receptor gamma(PPARG), which encodes the key adipogenic transcription factor peroxisome proliferator-activated receptor gamma(PPARγ). Clinical diagnosis is challenging due to phenotypic overlap with common metabolic syndromes. We identified a novel PPARG variant in a Chinese family and performed comprehensive functional characterization to elucidate its pathogenic mechanism. The proband, a 15-year-old boy presenting with atypical fat distribution, severe insulin resistance, hypertriglyceridemia, and pancreatitis, underwent clinical evaluation and whole-exome sequencing. The identified variant was confirmed by Sanger sequencing. Its functional impact was assessed through in silico modeling, luciferase reporter assays, protein stability analysis (cycloheximide chase), and evaluation of mitochondrial function (JC-1 staining) and adipocyte gene expression in cellular models. A heterozygous PPARG c.634C>T (p.Arg212Trp, R212W) variant was identified and segregated with the phenotype. Functional studies revealed that the R212W mutant exhibits a partial loss of transcriptional activity (~40% of wild-type) while retaining ligand sensitivity. Crucially, we demonstrated that the mutant protein has significantly reduced stability due to accelerated degradation. In adipocyte models, R212W expression led to impaired mitochondrial membrane potential, depleted cellular ATP levels, and downregulated expression of key metabolic genes (glucose transporter 4[GLUT4], adiponectin[ADIPOQ], fatty acid binding protein 4[FABP4], lipoprotein lipase[LPL], perilipin 1[PLIN1]). These functional deficits were partially rescued by treatment with the PPARγ agonist rosiglitazone. We report a novel pathogenic PPARG R212W variant associated with FPLD3. Our data extend beyond a simple loss-of-function model by establishing a multi-faceted pathogenic mechanism involving protein destabilization, mitochondrial dysfunction, and cellular bioenergetic failure. The partial rescue by rosiglitazone suggests a potential therapeutic avenue. This study underscores the importance of integrating clinical phenotyping with deep functional analysis to diagnose and understand rare monogenic lipodystrophies.

#5

Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells.

American journal of physiology. Lung cellular and molecular physiology2026 Apr 01

Pulmonary hypertension (PH) is a progressive vascular disease driven by pulmonary arterial remodeling, characterized by cellular hyperproliferation, resistance to apoptosis, and phenotypic plasticity. Our laboratory has shown that the proton-gated cation channel, acid-sensing ion channel 1a (ASIC1a), is essential for the development of chronic hypoxia (CH)-induced PH in rodents. Importantly, ASIC1a activation occurs without changes in total ASIC1a levels but reflects a hypoxia-dependent redistribution to the plasma membrane in pulmonary arterial smooth muscle cells (PASMCs). In neurons, mitochondrial-localized ASIC1a (mtASIC1a) contributes to oxidative stress-induced mitochondrial membrane potential (ΔΨm) depolarization and apoptosis. Although mtASIC1a has not been described in vascular cells, its role in PASMCs may be relevant to mitochondrial dysfunction and apoptosis resistance in PH. We hypothesize that mtASIC1a is a crucial regulator of PASMC mitochondrial homeostasis, and its loss following CH promotes mitochondrial dysfunction and apoptosis resistance. Consistent with this, mtASIC1a localization was decreased in PASMCs and intrapulmonary arteries from CH rats compared with controls. Functionally, PASMCs from CH rats or Asic1a knockout mice exhibited ΔΨm hyperpolarization, elevated mitochondrial Ca2+ and superoxide, impaired mitophagy, and reduced cleaved caspase-3. Transmission electron microscopy revealed mitochondrial morphological changes, including increased size and circularity, decreased aspect ratio, and reduced mitochondrial number per cell, whereas fusion/fission proteins remained largely unchanged. Lentiviral restoration of mtASIC1a prevented ΔΨm hyperpolarization and restored caspase-3 cleavage. These findings identify mtASIC1a as a novel regulator of mitochondrial function in PASMCs, where its loss following CH promotes ΔΨm hyperpolarization, impaired mitophagy, and resistance to apoptosis.NEW & NOTEWORTHY This study identifies mitochondrial acid-sensing ion channel 1a (mtASIC1a) as a novel regulator of mitochondrial homeostasis in pulmonary arterial smooth muscle cells (PASMCs). Critically, mtASIC1a deficiency in PASMCs following in vivo chronic hypoxia or genetic deletion promotes mitochondrial membrane potential (ΔΨm) hyperpolarization, Ca2+ and superoxide (O2-) accumulation, impaired mitophagy, and caspase inhibition. Restoring mtASIC1a by lentiviral transduction prevents ΔΨm hyperpolarization and restores caspase cleavage, highlighting its importance in mitochondrial signaling and hypoxic pulmonary hypertension pathophysiology.

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Ver todas no PubMed

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The VPS35 protein and the role of its impairments in mitochondrial dysfunction in Parkinson's disease.

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Mitochondrial Iron Handling and Lipid Peroxidation as Drivers of Ferroptosis.

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Effects of Cannabidiol on TAFAZZIN-Deficient B-Lymphoblastoid Cells.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
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18β-Glycyrrhetinic acid attenuates endoplasmic reticulum stress and neuroinflammation via the PI3K/AKT-dependent pathway in MPTP/p-induced Parkinson's disease mouse model.

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Seasonal trade-offs shape metabolomic and proteomic responses to Varroa destructor parasitisation in honey bees (Apis mellifera).

Insect biochemistry and molecular biology
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Hypermethylation of FGF13 Reduces Microtubule Stability via Interaction With TUBB2A to Promote Mitochondrial Dysfunction in Alzheimer's Disease.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
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In Vitro Evaluation of Cadmium-Induced Phosphate Reabsorption Impairment.

Journal of applied toxicology : JAT
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A Heteroplasmic MT-CO2 m.8024G > A Variant Is Associated with Mitochondrial Bioenergetic Deficiency and Optic Atrophy.

Molecular neurobiology
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The genetic architecture of postoperative delirium after major surgery and its relationship with nonpostoperative neurocognitive conditions: A genome-wide association study.

PLoS medicine
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N-acetyl-l-leucine lowers α-synuclein levels and improves synaptic function in Parkinson's disease models.

The Journal of clinical investigation
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RNA-seq analysis reveals altered gene expression profiles in HMEC-1 cells overexpressing KRAS gene associated with brain arteriovenous malformation.

Chinese neurosurgical journal
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ITPR2 Promotes Acute Myeloid Leukemia Progression Through Calcium-Mediated Mitochondrial Dysfunction.

Frontiers in bioscience (Landmark edition)
2026

Lithium chloride suppresses ferroptosis of induced pluripotent stem cells with ApoE4/E4 from a sporadic Alzheimer's disease patient.

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
2026

A Novel PPARG R212W Variant Causes Familial Partial Lipodystrophy Type 3: Clinical Presentation and Functional Characterization.

International journal of molecular sciences
2026

Unraveling GDAP1: Bridging Mitochondrial Biology and Peripheral Neuropathy.

Biomolecules
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Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells.

American journal of physiology. Lung cellular and molecular physiology
2026

Targeting VDAC1-dependent mtDNA release attenuates fibroblast innate immune activation and vitiligo pathogenesis.

International immunopharmacology
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Candida auris vacuolar calcium pump mediates fluconazole efflux and resistance evolution.

Nature microbiology
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ALDH2 activation protects against mutant TOMM40-mediated mitochondrial dysfunction and neurodegeneration in Alzheimer's disease.

Life sciences
2026

BRD4-mediated ER membrane contact creates functionally distinct mitochondrial subtypes.

Molecular cell
2026

Mitochondrial calcium uniporter knockdown in hippocampal neurons effectively attenuates synaptic plasticity impairment and pathology in APP/PS1/tau model of Alzheimer's disease.

Experimental neurology
2026

MFN2-CD36 interaction regulates mitochondrial lipid digestion in cancer-associated fibroblasts and promotes esophageal squamous cell carcinoma progression.

Cancer letters
2026

Ferrostatin-1 attenuates sepsis-induced lung injury by inhibiting ferroptosis via activation of the SLC7A11/GSH/GPX4 signaling pathway.

Journal of chromatography. B, Analytical technologies in the biomedical and life sciences
2026

Soluble ST2 drives fulminant myocarditis progression via the IGF2R-YY1 mitochondrial axis.

European heart journal
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DIDS modulates VDAC1 oligomerization to suppress intrinsic apoptosis and attenuates in vitro and in vivo RSV infection.

Journal of virology
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Mitochondrial dysfunction and applications of mitochondrial-targeted delivery systems in atherosclerosis.

Drug delivery
2026

Statins halt polycystic liver disease by reprogramming metabolism and normalizing mitochondrial bioenergetics in cystic cholangiocytes.

Hepatology (Baltimore, Md.)
2026

Selenium Nanoparticles Protect Retinal Pigment Epithelial Cells Against Experimental Age-Related Macular Degeneration-Induced Mitochondrial Oxidative Toxicity and Apoptosis Through the Modulation of the TRPM2 Channel.

Journal of biochemical and molecular toxicology
2026

Sialin-STAT3 axis regulates bone homeostasis in mice.

Bone research
2025

[Heterogeneity in the regulation of cellular stress responses by FUS gene mutations associated with amyotrophic lateral sclerosis].

Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
2026

A dynamic displacement mechanism drives protein import into mitochondria.

bioRxiv : the preprint server for biology
2026

Amyloid precursor protein interacts with the mitochondrial phosphatase PGAM5 and regulates mitochondrial respiration.

bioRxiv : the preprint server for biology
2026

Transient protein structure guides surface diffusion pathways for electron transport in membrane supercomplexes.

Nature communications
2026

SIRT3 attenuates chronic pain-induced depressive-like behaviors by deacetylating CypD at lysine 166 in central amygdala.

European journal of pharmacology
2026

ZFT is the major iron and zinc transporter in Toxoplasma gondii.

eLife
2026

Taurochenodeoxycholic Acid Activates Calcium Signaling to Protect Against Fuchs' Endothelial Corneal Dystrophy.

Investigative ophthalmology &amp; visual science
2026

Lactate-driven ATP6V1B2 lactylation triggers asthmatic inflammation by linking lysosomal dysfunction to mitochondrial ROS-dependent pyroptosis.

Redox biology
2026

Kisspeptin improves local ovarian insulin resistance in PCOS by modulating the PI3K/AKT/GLUT4 signaling pathway.

PloS one
2026

Inhibition of TRPV4 Regulates Mitophagy Through the Sirt1/FoxO1 Signaling Pathway To Alleviate Acute Lung Injury.

Inflammation
2026

The possible mechanism of L-arginine improved intestinal barrier health in grass carp (Ctenopharyngodon idella): via suppressing apoptosis and enhancing mitochondria-endoplasmic reticulum crosstalk.

Free radical biology &amp; medicine
2026

Newcastle disease virus hijacks mitophagy to reprogram amino acid metabolism for enhanced replication.

Autophagy
2026

Mitochondria-targeted antioxidant AntiOxBEN2 prevents metabolic dysfunction-associated steatotic liver disease (MASLD) by enhancing fatty acid oxidation and mitochondrial bioenergetics.

Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie
2026

Aberrant skeletal muscle morphogenesis and myofiber differentiation characterize equine myotonic dystrophy.

PloS one
2026

The association of Alzheimer's disease-related SNPs with mild cognitive impairment susceptibility in the Chinese population.

Scientific reports
2026

Sinomenine inhibits oxidative stress to attenuate Alzheimer's disease pathology via α7 nicotinic acetylcholine receptor.

Phytomedicine : international journal of phytotherapy and phytopharmacology
2026

BAM 15 Exerts Molluscicidal Effects on Pomacea canaliculata Through the Induction of Oxidative Stress, Impaired Energy Metabolism, and Tissue Damage.

Molecules (Basel, Switzerland)
2026

Collapsin Response Mediator Protein 2 (CRMP2) Modulates Induction of the Mitochondrial Permeability Transition Pore in a Knock-In Mouse Model of Alzheimer's Disease.

Cells
2026

Investigating the Potential Role of Capsaicin in Facilitating the Spread of Coxsackievirus B3 via Extracellular Vesicles.

International journal of molecular sciences
2026

Cystinosis and Cellular Energy Failure: Mitochondria at the Crossroads.

International journal of molecular sciences
2026

Choline Deficiency Drives the Inflammation-Fibrosis Cascade: A Spatiotemporal Atlas of Hepatic Injury from Weeks 6 to 10.

Antioxidants (Basel, Switzerland)
2026

Influence of drying temperature on the metabolites profile and potential antioxidant pathways of Passiflora edulis peel: Integrating untargeted metabolomics with network pharmacology analyses, molecular docking, and molecular dynamics simulation.

Computational biology and chemistry
2026

Blood Flow Regulates Metabolism in Hematopoietic Development.

Advances in experimental medicine and biology
2026

MPC1 deficiency promotes melanoma progression via Wnt/β-catenin signaling.

Biochemical and biophysical research communications
2026

Impact of Toll/Interleukin-1 Receptor Domain Protein C on Mesenchymal Stem Cells Mitochondrial Protein Expression: A Proteomic Study.

Current molecular medicine
2026

Itaconate and its derivatives ameliorate autoimmunity by suppressing Th17 cells via regulating mitophagy.

Cell communication and signaling : CCS
2026

METTL16-m6A-PGC-1α axis contributes to exercise-induced mitochondrial adaptations in skeletal muscle of high-fat diet-fed insulin-resistant mice.

BMC biology
2026

Immunohistochemical Analysis of Tom20 in Choroid Plexus Epithelial Cells From Elderly Brains With Neurodegenerative Diseases.

Neuropathology : official journal of the Japanese Society of Neuropathology
2026

VPS13A Deficiency Leads to Impaired Lipid Distribution and Alteration of Mitochondrial Calcium Homeostasis in Fibroblasts of VPS13A Disease Patients.

Movement disorders : official journal of the Movement Disorder Society
2025

The role of gasdermin-mediated mitochondrial RNA release in amplifying secondary immune response during microbial infection.

Frontiers in immunology
2026

A small molecule VDAC ligand inhibits ERAD and induces selective cancer cell death via disruption of calcium homeostasis.

Nature communications
2026

Signaling architecture of the glucagon-like peptide-1 receptor.

The Journal of clinical investigation
2026

Tmem110 regulates the conformation of TRPML1 to maintain endolysosomal homeostasis and prevent mitochondrial DNA leakage and pathological self-DNA processing.

Nature communications
2026

Mitochondrial DNA 6 mA methylation by METTL4 drives neuroinflammation via cGAS-STING activation in vascular cognitive impairment.

Free radical biology &amp; medicine
2026

TOM70-Mitochondrial Pathway Reduction Mediates DEHP-Induced Neuroinflammation in Mice.

Journal of agricultural and food chemistry
2026

Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.

Apoptosis : an international journal on programmed cell death
2026

Parkin Deficiency Impairs ER-Mitochondria Associations and calcium homeostasis via IP3R-Grp75-VDAC1 Complex.

International journal of biological sciences
2026

Non-surgical periodontal treatment improves mitochondrial bioenergetics in circulating immune cells of patients with chronic periodontitis.

Free radical biology &amp; medicine
2026

Clonidine compromises human sperm functions.

Reproductive toxicology (Elmsford, N.Y.)
2025

Interplay Between 3D Chromatin Architecture and Gene Regulation at the APOE Locus Contributes to Alzheimer's Disease Risk.

International journal of molecular sciences
2025

[Research advances in key mitochondrial injury targets and mechanisms of traditional Chinese medicine intervention in ischemic stroke].

Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
2026

Neuroprotective effect of Saikogenin F on corticosterone-induced cytotoxicity in PC12 cells involves P2X7R-NLRP3 and cAMP-PKA pathways.

In vitro cellular &amp; developmental biology. Animal
2026

Müller Glial Kir4.1 Channel Dysfunction in APOE4-KI Model of Alzheimer's Disease.

Glia
2026

Endothelial mitochondrial dysfunction in hypertension, diabetes, and atherosclerosis.

Cardiovascular research
2025

The ion transport, GPCR, and RTK toolkit expression in the human cerebrovascular endothelial cell line, hCMEC/D3: an Omics perspective.

Frontiers in physiology
2026

Elevated cerebrospinal fluid 2-Hydroxybutyric acid in two siblings with aspartate-glutamate carrier 1 deficiency.

Molecular genetics and metabolism
2026

Ginsenoside-based nanoliposomes co-delivering ergothioneine and coenzyme Q10 to combat skin aging via mitochondrial modulation.

Colloids and surfaces. B, Biointerfaces
2025

Pridopidine, a Potent and Selective Therapeutic Sigma-1 Receptor (S1R) Agonist for Treating Neurodegenerative Diseases.

Pharmaceuticals (Basel, Switzerland)
2026

Overexpression of mitofusin 2 ameliorates inflammation and oxidative stress in lipopolysaccharide-induced mastitis model by regulating phosphofurin acidic cluster sorting protein 2.

Animal models and experimental medicine
2025

Mitochondria-associated endoplasmic reticulum membranes and calcium ion exchange: A novel direction for aging and neurodegenerative diseases.

Neural regeneration research
2025

Trigger points of palliative care assessment in inherited metabolic diseases.

Orphanet journal of rare diseases
2025

Canagliflozin Promotes Structural and Functional Changes in Proximal Tubular Cell Mitochondria of Hypertensive-Diabetic Mice.

International journal of molecular sciences
2025

The Diagnostic Reliability of BIN1 and TOMM40 Genotyping in Assessing Dementia Risk.

Genes
2025

Growth Hormone Response in a Child With a Homozygous TOMM7 Mutation: Novel Therapeutic Insights.

The American journal of case reports
2025

[PNPLA3 gene I148M polymorphism induces hepatic fibrosis via cholesterol metabolic dysregulation in mice].

Sheng wu gong cheng xue bao = Chinese journal of biotechnology
2025

TMAO converts cytochrome c into a pro-apoptotic peroxidase by destabilizing the heme-Met80 ligation.

Cellular and molecular biology (Noisy-le-Grand, France)
2026

Synuclein and Mitochondrial Dysfunction: Regulating the Protein Import Complex toward PD Treatment?

ACS chemical neuroscience
2025

Inhibin beta A drives colorectal cancer progression through macrophage M2 polarization and mitochondria-dependent ferroptosis suppression.

Signal transduction and targeted therapy
2025

Multiomics Integration Reveals a Metabolic Myopathy in Cardiometabolic HFpEF.

bioRxiv : the preprint server for biology
2025

[Exploring the potential causes of sarcopenia in sepsis patients based on proteome sequencing].

Zhonghua wei zhong bing ji jiu yi xue
2025

Mitochondrial DNA release via mPTP and BAX/BAK drives inflammatory injury in intestinal ischemia reperfusion.

Cell communication and signaling : CCS
2026

LRRC8A Mediates Ischemic Neuronal Injury by Potentiating NMDA Receptor Activity and Activating Mitochondrial Apoptotic Pathway.

Cell biology international
2025

Beyond oxidative stress: Ferroptosis as a novel orchestrator in neurodegenerative disorders.

Frontiers in immunology
2026

Synaptotagmin-7 drives stress-induced cardiomyocyte necroptosis via the p53-Bak-mPTP axis.

Theranostics
2025

VDAC1: at the crossroads of cancer signalling and metabolism.

Expert review of proteomics
2026

Biallelic FOXRED1 mutations cause infantile mitochondrial encephalopathy with complex I disassembly and basal ganglia degeneration.

Mitochondrion
2025

Hypoxic Mesenchymal Stem Cell Exosome-Derived SLC25A3 Ameliorates Bronchopulmonary Dysplasia by Modulating Macrophage Polarization and Oxidative Stress.

Cell biochemistry and function
2026

GRP75 blocks hepatitis E virus infection by targeting HEV-ORF2 for degradation through chaperone-mediated autophagy and promoting IRF3 activation.

Journal of virology
2025

Hv1 inhibition rescues AD pathology by restoring microglial mitochondrial function and enhancing mitochondrial transfer.

Experimental &amp; molecular medicine
2025

VPS13B recruits lipid vesicles to promote mitochondrial fission and quality control.

Nature communications
2026

Investigating Mitochondrial Viscosity in Ferroptosis-Mediated Drug-Induced Liver Injury using a Double-Targeted Strategy.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)
2026

α7 Nicotinic acetylcholine receptor activation rescues mitochondrial dysfunction in gestational diabetes mellitus by competing with p66Shc for VDAC1 binding.

Diabetologia
2025

RHOA regulates mitochondria-ER contact sites through modulation of the VAPB/PTPIP51 tether.

Nature communications
2026

Time-specific perturbation of the serotonergic system differentially modulates the transcriptional landscape of hippocampal subregions in female rats.

Biochemical pharmacology
2026

Small Extracellular Vesicles From Human Amniotic Membrane Mesenchymal Stem Cells Rejuvenate Senescent β Cells and Cure Age-Related Diabetes in Mice.

Aging cell
2025

Engineered extracellular vesicles-mediated curcumin delivery in brain microenvironment modulating lysosomes, mitochondria, and microglia reprogram for parkinson's disease therapy.

Journal of nanobiotechnology
2026

Assessment of SLC25A46 variants in idiopathic Parkinson's disease.

Parkinsonism &amp; related disorders
2026

Hyperbaric oxygen targets RCN1 to modulate ER-mitochondria crosstalk and ameliorate sorafenib resistance in hepatocellular carcinoma.

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
2025

Extracellular Vesicles from iPSC-Derived Glial Progenitor Cells Prevent Glutamate-Induced Excitotoxicity by Stabilising Calcium Oscillations and Mitochondrial Depolarisation.

Cells
2025

The role of mitochondrial-associated endoplasmic reticulum membranes (MAMs) in diabetic microvascular complications: a review.

Cell death &amp; disease
2026

Rationally engineered cyclodextrins: smart shuttles for neurological drug targeting and BBB modulation.

Bioorganic chemistry
2026

ATG9A-PLA2G6 axis reprograms phospholipid metabolism to drive metabolic liver disease and hepatocellular carcinoma.

Autophagy
2026

Three mammalian VDAC isoforms distinctly regulate mitochondrial function and proteome to maintain cell metabolism.

The Journal of biological chemistry
2025

TRIP13 alters mitochondrial function and promotes bortezomib resistance in multiple myeloma.

Scientific reports
2026

Structural transport and inhibition mechanism of the mitochondrial pyruvate carrier.

Trends in biochemical sciences
2026

Stress at the gates: Mitochondrial import dysfunctions, response pathways, and therapeutic potential.

Mitochondrion
2025

The role of FIS1 and its post-translational modifications in diseases and health damage caused by environmental pollution.

Cell biology and toxicology
2025

Mechanisms and treatment modalities related to premature ovarian insufficiency in mitochondria: literature review.

Journal of ovarian research
2026

ABCC9 knockdown attenuates isoproterenol‑induced myocardial hypertrophy by inhibiting the PI3K/AKT signaling pathway.

Molecular medicine reports
2025

Mitochondria-targeted gene delivery using fluorinated lipid nanoparticles to alleviate Leber's hereditary optic neuropathy.

Nature communications
2026

Mitochondria in pyroptosis: Mechanisms and implications.

Molecular immunology
2025

Vacuolar-type H+-ATPase-mediated extra-organellar buffering resolves mitochondrial dysfunction.

Nature communications
2025

Transcriptome-Wide N7-Methylguanosine (m7G) Map Profiling Reveals the Regulatory Role of m7G in Atherosclerosis.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
2026

Integrated multi-omics and machine learning elucidate the pathogenic role of mitophagy in osteoarthritis and identify novel therapeutic strategies.

International immunopharmacology
2026

Enhanced S-Palmitoylated Protein Detection by Mild Nonionic Detergent in Proteomic Workflow.

Journal of the American Society for Mass Spectrometry
2025

Ceftriaxone alleviates mitochondrial damage through the inhibition of extrasynaptic NMDA receptor-mediated changes in intracellular calcium levels to improve cognitive deficits in APP/PS1 mice.

Alzheimer's research &amp; therapy
2025

Disruption of the PIKfyve complex unveils an adaptive mechanism to promote lysosomal repair and mitochondrial homeostasis.

Nature communications
2025

Membrane Trafficking in Psychiatric Disorders: Bridging Cellular Dysfunction and Mental Health-A Narrative Review.

Molecular neurobiology
2026

Glutathione and TRPM2 Inhibition Reduce Amyloid-Beta and Lipopolysaccharide-Induced Apoptosis, Inflammation, and Oxidative Stress in Microglial Cells.

Cell biology international
2025

N-terminal α-amino SUMOylation promotes phosphorylation-independent cofilin-1 translocation to the mitochondrial matrix and induces apoptosis.

Nature communications
2025

Altered Co-Expression Patterns of Mitochondrial NADH-Dehydrogenase Genes in the Prefrontal Cortex of Rodent ADHD Models.

International journal of molecular sciences
2025

Targeting TOMM40 and TOMM22 to Rescue Statin-Impaired Mitochondrial Function, Dynamics, and Mitophagy in Skeletal Myotubes.

International journal of molecular sciences
2025

CISD2 ensures adequate ER-mitochondrial coupling, critically supporting mitochondrial function in neurons.

Acta neuropathologica communications
2025

Naringenin alleviates endotoxin-induced acute kidney injury in chicken by inhibiting pyroptosis through PINK1-dependent mitophagy.

Phytomedicine : international journal of phytotherapy and phytopharmacology
2026

SodA promotes immune evasion of Streptococcus suis by suppressing ROS accumulation and GSDMD-mediated mitochondrial disruption in neutrophils.

Microbiology spectrum
2025

Loss-of-function variant of SLC27A3 causes mitochondrial dysfunction and a metabolic neurodevelopmental disorder via impaired fatty acid transport.

Journal of human genetics
2025

Regulation of mitochondrial dynamics and function by melatonin type 1 receptor in parkinson's disease.

Cellular and molecular life sciences : CMLS
2026

Altered dimerization of certain riboflavin transporter 2 mutants: a possible source of UPR, altered calcium signalling and mitochondrial derangements in RTD2.

Archives of biochemistry and biophysics
2025

Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
2026

Mitochondrial protein TOMM7 alleviates diabetic kidney disease by regulating mitophagy via intracellular redistribution of phospholipase PLA2G6.

Kidney international
2026

Sirtuin downregulation mediates mitochondrial impairment causing cognitive decline in hepatic encephalopathy.

Free radical biology &amp; medicine
2025

MICU2 controls mitochondrial calcium signaling and migration in neurons during development.

Cell reports
2026

Mechanistic study of the cytotoxicity of cannabidiol and its metabolites in HepG2 cells.

Archives of toxicology
2026

A unified mechanism for mitochondrial damage sensing in PINK1-Parkin-mediated mitophagy.

The EMBO journal
2025

The dynamic lateral gate of the mitochondrial β-barrel biogenesis machinery is blocked by darobactin A.

Nature communications
2026

Sphingosine-1-phosphate activates ICl,swell in ventricular myocytes via mitochondrial reactive oxygen production.

Journal of molecular and cellular cardiology
2025

Oxidative modification of G-quadruplex triggers CLIC4-associated mitochondrial dysfunction to promote glioblastoma progression.

Redox biology
2026

Elamipretide: The first cardiolipin-directed mitochondrial therapeutic for Barth syndrome approved under accelerated approval.

Drug discoveries &amp; therapeutics
2025

Pathogenic KIF5C mutation disrupts dendritic spine maturation and mitochondrial trafficking in neurodevelopmental disorders.

Neurobiology of disease
2025

Failure of lysosomal acidification and endomembrane network in neurodegeneration.

Experimental &amp; molecular medicine
2025

Sodium hexametaphosphate mitigates calcium oxalate stone formation by modulating crystallization and maintaining PPARα signaling.

Urolithiasis
2025

Amyloid-beta glycation induces neuronal mitochondrial dysfunction and Alzheimer's pathogenesis via VDAC1-dependent mtDNA efflux.

Proceedings of the National Academy of Sciences of the United States of America
2025

The sigma-1 receptor as a neurohomeostatic decision hub for GABARAP-mediated receptor trafficking and macroautophagy.

Frontiers in molecular biosciences
2025

Mitochondrial cristae remodeling: Mechanisms, functions, and pathology.

Cell insight
2026

Elucidating the Localization and Interactome of Mitochondrial Microproteins.

Methods in molecular biology (Clifton, N.J.)
2025

Mitochondrial Calcium Channels and MAM Interaction in Calcium Homeostasis Dysregulation in Parkinson's Disease.

Neurochemical research
2025

MPTP mediated Ox-mtDNA release inducing macrophage pyroptosis and exacerbating MCD-induced MASH via promoting the ITPR3/Ca2+/NLRP3 pathway.

Journal of translational medicine
2025

Glycerol-3-phosphate activates ChREBP, FGF21 transcription and lipogenesis in citrin deficiency.

Nature metabolism
2025

The transcription factor HAND1 suppresses endometrial cancer progression by regulating fatty acid β-oxidation via c-MET.

International journal of biological macromolecules
2026

Glutaredoxin 2 is essential for AML survival through mitochondrial permeability transition pore regulation.

Blood
2026

Multisite, Multiancestry Genome-Wide Association Study Meta-Analysis of Functional Seizure Disorder in a Hospital Sample of 675,680 Patients.

Biological psychiatry global open science
2026

The roles of glycerophospholipids in the aging retina and age-related macular degeneration.

Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
2026

Mitochondrial Metabolic Reprogramming of Cortical Neurons by Prenatal Exposure to Corticosterone: A Shift from ATP Synthesis to Membrane Potential Maintenance.

Experimental neurobiology
2025

Potent Preorganized Pyrazolidine Cyclophilin D Inhibitors Prevent Mitochondrial and Organ Injury in a Mouse Pancreatitis Disease Model.

Journal of medicinal chemistry
2026

Protein-Mediated Virulence in Mycobacterium tuberculosis.

Advances in experimental medicine and biology
2025

Cinchona-based liquid formulation exhibits antifungal activity through Tryptophan starvation and disruption of mitochondrial respiration in Rhizoctonia Solani.

Scientific reports
2025

Dexmedetomidine protects against postoperative neurocognitive disorder by mitigating mitochondrial dysfunction through regulating the IP3R-GRP75-VDAC1 complex-mediated calcium transport.

Immunologic research
2025

Membrane IL-18 identifies a human macrophage subset with distinct proteomic and functional traits.

Oncoimmunology
2025

Impaired cardiac non-neuronal acetylcholine synthesis triggers mitochondrial dysfunction with the loss of nicotinic receptor-mediated calcium handling, causing the failing heart.

Clinical science (London, England : 1979)
2025

A novel palmitoylation-based molecular signature reveals COX6A1 as a key regulator in metabolic dysfunction-associated steatotic liver disease.

Journal of translational medicine
2025

Cell-type-specific dysregulation of mitochondrial calcium signaling in Alzheimer's disease.

Cell communication and signaling : CCS
2025

Cytochrome c Oxidase Subunit 5A (COX5A) Enhances Gastric Cancer Progression by Augmenting ATP Synthesis and Activating the PI3K/Akt Pathway.

Journal of cellular and molecular medicine
2026

Mitochondrial NOX4 drives atrial fibrillation via redox-dependent structural remodeling and fibrosis.

Free radical biology &amp; medicine
2025

p53-mediated regulation of electron transport chain and nucleotide synthesis during Newcastle disease virus infection.

Journal of virology
2025

Eliosin-an alternative product from the HmPKD1 locus is a component of endoplasmic reticulum mitochondria membrane contact sites.

PloS one
2025

Empagliflozin-pretreated BMSC exosomes attenuate myocardial ischemia-reperfusion injury by enhancing atad3a/pink1-dependent mitophagy.

Stem cell research &amp; therapy
2026

Longevity-promoting mitochondrial unfolded protein response activation requires elements of the PeBoW complex.

Genes &amp; development
2025

Linking brain entropy to molecular and cellular architecture in psychosis.

NeuroImage
2025

Mitochondrial Fragmentation Induced by the CFTR Modulators Lumacaftor and Ivacaftor in Immortalized Cystic Fibrosis Cell Lines.

Cells
2025

MPC-mediated lactate production drives histone lactylation in dendritic cells to affect tumor progression and immunotherapy.

Cellular and molecular life sciences : CMLS
2025

Pleiotropic Actions of Gastrodia Elata Glucosides in the Treatment of Painful Neuropathies and CNS Disorders: Focus on Mitochondrial Dysfunction and Modulation of Ion Channels.

Current neuropharmacology
2025

Indole-3-carbinol is an inhibitor of KV1.3 potassium voltage-gated channel activity in chronic lymphocytic leukemia cells.

European journal of pharmacology
2025

Human dental pulp stem cell-derived mitochondria restore mitochondrial function and promote neuroregeneration in a cellular model of Parkinson's disease.

Stem cell research &amp; therapy
2025

Identification and functional analysis of circular RNAs during mitochondrial damage induced by infectious bovine rhinotracheitis virus infection in Madin-Darby bovine kidney cells.

BMC genomics
2026

TbTim20 facilitates protein import at a low membrane potential in trypanosomes lacking the mitochondrial genome.

The FEBS journal
2025

Mitochondrial dysfunction, reactive oxygen species, and diabetes mellitus - A triangular relationship: A review.

Biomolecules &amp; biomedicine
2025

Increased Intermembrane Space [Ca2+] Drives Mitochondrial Structural Damage in CPVT.

Circulation research
2026

FLVCR1 Deficiency Impairs Mitochondrial Homeostasis in Retinal Degeneration: Choline as a Potential Therapy.

Clinical &amp; experimental ophthalmology
2025

From loss of Ca2+-influx to altered organelle temperature and energy failure: A neonatal-lethal TRPV4 mutant (L618P).

Life sciences
2025

Unlocking Neuroprotection: Simultaneous Suppression of Mitochondrial Energetic Collapse and Oxidative-Inflammatory Vortex for Ischemia-Reperfusion Brain Injury.

ACS nano
2025

Mitochondrial proteomics reveals the impact of Estrogen in enhancing energy metabolism of patient-derived fibroblast-like synoviocytes in rheumatoid arthritis.

Inflammation research : official journal of the European Histamine Research Society ... [et al.]
2025

ZC3H4, a novel regulator of mitochondrial complex I, impacts prostate stromal cell senescence, attachment, adhesion and anoikis resistance.

Cell death &amp; disease
2025

Structural dynamics of the mitochondrial ADP/ATP carrier support an asymmetric transport mechanism.

International journal of biological macromolecules
2025

Mini-review: "Hippocalcin: Molecular mechanisms and therapeutic potential in neuronal function".

Neuroscience letters
2025

Sex dimorphism and substrate dependency of liver mitochondrial bioenergetics and H2O2 production.

American journal of physiology. Gastrointestinal and liver physiology
2025

The Steroidogenic Acute Regulatory (STAR) Gene Anatomy, Expression, and Roles.

Development &amp; reproduction
2025

Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.

Journal of translational medicine

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Doenças relacionadas

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Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Mitochondrial Iron Handling and Lipid Peroxidation as Drivers of Ferroptosis.
    International journal of molecular sciences· 2026· PMID 41828457mais citado
  2. The genetic architecture of postoperative delirium after major surgery and its relationship with nonpostoperative neurocognitive conditions: A genome-wide association study.
    PLoS medicine· 2026· PMID 41770756mais citado
  3. ITPR2 Promotes Acute Myeloid Leukemia Progression Through Calcium-Mediated Mitochondrial Dysfunction.
    Frontiers in bioscience (Landmark edition)· 2026· PMID 41761959mais citado
  4. A Novel PPARG R212W Variant Causes Familial Partial Lipodystrophy Type 3: Clinical Presentation and Functional Characterization.
    International journal of molecular sciences· 2026· PMID 41751985mais citado
  5. Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells.
    American journal of physiology. Lung cellular and molecular physiology· 2026· PMID 41740252mais citado
  6. Targeting SLC25A33 Suppresses Vascular Smooth Muscle Cell Proliferation and Migration by Reducing Cytosolic mtDNA Levels: Implications for Occlusive Vascular Diseases.
    Diabetes Metab J· 2026· PMID 40734498recente
  7. The depletion of TFAM and p-β-catenin(S552) in mitochondria in response to BoAHV-1 productive infection leads to decreased mitochondrial biogenesis.
    Vet Microbiol· 2025· PMID 40073611recente
  8. SLC25A48 influences plasma levels of choline and localizes to the inner mitochondrial membrane.
    Mol Genet Metab· 2024· PMID 39047301recente
  9. Screening mitochondria-related biomarkers in skin and plasma of atopic dermatitis patients by bioinformatics analysis and machine learning.
    Front Immunol· 2024· PMID 38774875recente
  10. Pathological Sequelae Associated with Skeletal Muscle Atrophy and Histopathology in G93A*SOD1 Mice.
    Muscles· 2023· PMID 38516553recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:254827(Orphanet)
  2. MONDO:0016800(MONDO)
  3. GARD:20761(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Q55786458(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

Doença do transporte membranar mitocondrial
Compêndio · Raras BR

Doença do transporte membranar mitocondrial

ORPHA:254827 · MONDO:0016800
CID-11
MedGen
UMLS
C5680718
Wikidata
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