ArticleJACC. Cardiovascular imaging2011
Adenine nucleotide translocase 1 deficiency results in dilated cardiomyopathy with defects in myocardial mechanics, histopathological alterations, and activation of apoptosis.
Article in JACC. Cardiovascular imaging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 61 citations in OpenAlex.
- Mitochondrial cardiomyopathy: bridging molecular mechanisms and clinical frontiers.Nature reviews. Cardiology · 2026Review
- Partial restoration of mitochondrial dysfunction by AAV-Ant1 protects from dilated cardiomyopathy in Ant1Nature communications · 2025Article
- ANT1 suppression inhibits the progression of colorectal cancer by suppressing PINK1/Parkin-mediated mitophagy.Acta biochimica et biophysica Sinica · 2025Article
- Myocardial disarray drives metabolic inefficiency in human cardiomyocytes.Communications biology · 2025Article
- Adenine Nucleotide Translocase 1 Promotes Functional Integrity of Mitochondria via Activating DDIT3-CytC Pathway and Intensifying Actin Filament Structures.Molecular neurobiology · 2025Article
- A New Perspective on the Role of Alterations in Mitochondrial Proteins Involved in ATP Synthesis and Mobilization in Cardiomyopathies.International journal of molecular sciences · 2025Review
- Adenine nucleotide carrier protein dysfunction in human disease.IUBMB life · 2023Review
- Comprehensive Analysis of Mitochondrial Dynamics Alterations in Heart Diseases.International journal of molecular sciences · 2023Review
- Post-translational modifications and protein quality control of mitochondrial channels and transporters.Frontiers in cell and developmental biology · 2023Review
- Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management.Cells · 2022Review
- Mitochondrial energy metabolic transcriptome profiles during cardiac differentiation from mouse and human pluripotent stem cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- VDAC2 as a novel target for heart failure: CaCell calcium · 2022Review
- Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease.Cell death & disease · 2022Review
- Mitochondrial mutations alter endurance exercise response and determinants in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Adipose-derived mesenchymal stem cells preserve cardiac function via ANT-1 in dilated cardiomyopathy hamster model.Regenerative therapy · 2021Article
- ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson's disease model.Cell & bioscience · 2021Article
- Human-induced pluripotent stem cells for modelling metabolic perturbations and impaired bioenergetics underlying cardiomyopathies.Cardiovascular research · 2021Review
- An mtDNA mutant mouse demonstrates that mitochondrial deficiency can result in autism endophenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Regulation of the mitochondrial permeability transition pore and its effects on aging.Microbial cell (Graz, Austria) · 2020Article
- Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials.British journal of pharmacology · 2019Review
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9 authors at 2 institutions in 2 countries.
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Abstract
objectivesthe aim of this study was to test the hypothesis that chronic mitochondrial energy deficiency causes dilated cardiomyopathy, we characterized the hearts of age-matched young and old adenine nucleotide translocator (ANT)1 mutant and control mice.
backgroundANTs export mitochondrial adenosine triphosphate into the cytosol and have a role in the regulation of the intrinsic apoptosis pathway. Mitochondrial energy deficiency has been hypothesized, on the basis of indirect evidence, to be a factor in the pathophysiology of dilated cardiomyopathies. Ant1 inactivation should limit adenosine triphosphate for contraction and calcium transport, thereby resulting in early cardiac dysfunction with later dilation and heart failure.
methodswe conducted a multiyear study of 73 mutant (Ant1-/-) and 57 control (Ant1+/+) mice, between the ages of 2 and 21 months. Hearts were characterized by cardiac anatomy, echocardiographic imaging with velocity vector analysis, histopathology, and apoptosis assays.
resultsthe Ant1-/- mice developed a distinctive concentric dilated cardiomyopathy, characterized by substantial myocardial hypertrophy and ventricular dilation, with cardiac function declining earlier in age as compared to control mice. Left ventricular circumferential, radial, and rotational mechanics were reduced even in the younger mutants with preserved systolic function. Histopathologic analysis demonstrated increased myocyte hypertrophy, fibrosis, and calcification in the mutant mice as compared with control mice. Furthermore, increased cytoplasmic cytochrome c levels and caspase 3 activation were observed in the mutant mice.
conclusionsour results demonstrate that mitochondrial energy deficiency is sufficient to cause dilated cardiomyopathy, confirming that energy defects are a factor in this disease. Energy deficiency initially leads to early mechanical dysfunction before a decline in left ventricular systolic function. Chronic energy deficiency with age then leads to heart failure. Our results now allow us to use the Ant1-/- mouse model for testing new therapies for ANT1 mutant patients.
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