ArticleBiochimica et biophysica acta2016
Deficiency in the mouse mitochondrial adenine nucleotide translocator isoform 2 gene is associated with cardiac noncompaction.
Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Mitochondrial control of amino acid catabolism by a fasting-inducible mitochondrial carrier.Science advances · 2026Article
- Sirt5 preserves mitochondrial homeostasis to improve cardiac function in ischemia-reperfusion injury by inhibiting ANT2 lysine lactylation modification.Cellular and molecular life sciences : CMLS · 2026Article
- Mitochondrial cardiomyopathy: bridging molecular mechanisms and clinical frontiers.Nature reviews. Cardiology · 2026Review
- Review
- Partial restoration of mitochondrial dysfunction by AAV-Ant1 protects from dilated cardiomyopathy in Ant1Nature communications · 2025Article
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Metabolic reprogramming driven by Ant2 deficiency augments T Cell function and anti-tumor immunity in mice.Nature communications · 2025Article
- Investigating biomarkers of mitochondrial and aging-related genes in major depressive disorder through bioinformatics analysis.Frontiers in psychiatry · 2025Article
- ANT-Mediated Inhibition of the Permeability Transition Pore Alleviates Palmitate-Induced Mitochondrial Dysfunction and Lipotoxicity.Biomolecules · 2024Article
- Exosomal Preconditioning of Human iPSC-Derived Cardiomyocytes Beneficially Alters Cardiac Electrophysiology and Micro RNA Expression.International journal of molecular sciences · 2024Article
- Mitochondrial non-energetic function and embryonic cardiac development.Frontiers in cell and developmental biology · 2024Review
- Implications of Activating the ANT2/mTOR/PGC-1α Feedback Loop: Insights into Mitochondria-Mediated Injury in Hypoxic Myocardial Cells.Current issues in molecular biology · 2023Article
- ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy.Science advances · 2023Article
- Mitochondrial Volume Regulation and Swelling Mechanisms in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial Fission Process 1 controls inner membrane integrity and protects against heart failure.Nature communications · 2022Article
- VDAC2 as a novel target for heart failure: CaCell calcium · 2022Review
- Adenine nucleotide translocase regulates airway epithelial metabolism, surface hydration and ciliary function.Journal of cell science · 2021Article
- Mitochondria in Early Forebrain Development: From Neurulation to Mid-Corticogenesis.Frontiers in cell and developmental biology · 2021Review
- Regulation of the mitochondrial permeability transition pore and its effects on aging.Microbial cell (Graz, Austria) · 2020Article
- Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD.Science advances · 2019Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The mouse fetal and adult hearts express two adenine nucleotide translocator (ANT) isoform genes. The predominant isoform is the heart-muscle-brain ANT-isoform gene 1 (Ant1) while the other is the systemic Ant2 gene. Genetic inactivation of the Ant1 gene does not impair fetal development but results in hypertrophic cardiomyopathy in postnatal mice. Using a knockin X-linked Ant2 allele in which exons 3 and 4 are flanked by loxP sites combined in males with a protamine 1 promoter driven Cre recombinase we created females heterozygous for a null Ant2 allele. Crossing the heterozygous females with the Ant2(fl), PrmCre(+) males resulted in male and female ANT2-null embryos. These fetuses proved to be embryonic lethal by day E14.5 in association with cardiac developmental failure, immature cardiomyocytes having swollen mitochondria, cardiomyocyte hyperproliferation, and cardiac failure due to hypertrabeculation/noncompaction. ANTs have two main functions, mitochondrial-cytosol ATP/ADP exchange and modulation of the mitochondrial permeability transition pore (mtPTP). Previous studies imply that ANT2 biases the mtPTP toward closed while ANT1 biases the mtPTP toward open. It has been reported that immature cardiomyocytes have a constitutively opened mtPTP, the closure of which signals the maturation of cardiomyocytes. Therefore, we hypothesize that the developmental toxicity of the Ant2 null mutation may be the result of biasing the cardiomyocyte mtPTP to remain open thus impairing cardiomyocyte maturation and resulting in cardiomyocyte hyperproliferation and failure of trabecular maturation. This article is part of a Special Issue entitled 'EBEC 2016: 19th European Bioenergetics Conference, Riva del Garda, Italy, July 2-6, 2016', edited by Prof. Paolo Bernardi.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.