ArticleJournal of molecular medicine (Berlin, Germany)2016
Transgenic overexpression of adenine nucleotide translocase 1 protects ischemic hearts against oxidative stress.
Article in Journal of molecular medicine (Berlin, Germany), 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.
- Article
- Review
- Involvement of SIRT3 downstream targets ANT1, VDAC, CYPD, and Drp1 in a rat model of hepatic encephalopathy: Therapeutic role of thymoquinone.Iranian journal of basic medical sciences · 2026Article
- SLC25 in intestinal inflammation: mechanisms, pathological roles, and therapeutic implications.Frontiers in immunology · 2026Review
- Mitochondrial uncoupling, energy substrate utilization, and brown adipose tissue as therapeutic targets in cancer.npj metabolic health and disease · 2025Review
- Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence.Molecular oncology · 2025Article
- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- Mitochondrial Chronic Progressive External Ophthalmoplegia.Brain sciences · 2024Review
- An update of the molecular mechanisms underlying anthracycline induced cardiotoxicity.Frontiers in pharmacology · 2024Review
- Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases.International journal of molecular sciences · 2023Review
- Short-Term Blockade of Pro-Inflammatory Alarmin S100A9 Favorably Modulates Left Ventricle Proteome and Related Signaling Pathways Involved in Post-Myocardial Infarction Recovery.International journal of molecular sciences · 2022Article
- Perspectives on mitochondrial relevance in cardiac ischemia/reperfusion injury.Frontiers in cell and developmental biology · 2022Review
- Mitochondria Isolated from Hearts Subjected to Ischemia/Reperfusion Benefit from Adenine Nucleotide Translocase 1 Overexpression.Membranes · 2021Article
- Adenine Nucleotide Translocase 1 Expression Modulates the Immune Response in Ischemic Hearts.Cells · 2021Article
- ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson's disease model.Cell & bioscience · 2021Article
- Adenine nucleotide translocase regulates airway epithelial metabolism, surface hydration and ciliary function.Journal of cell science · 2021Article
- Article
- Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading.Cellular and molecular life sciences : CMLS · 2019Article
- The Role of Adenine Nucleotide Translocase in the Assembly of Respiratory Supercomplexes in Cardiac Cells.Cells · 2019Article
- Cytoplasmic upregulation of Cyto c and AIF serve as biomarkers of mechanical asphyxia death.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledIschemia impairs the adenine nucleotide translocase (ANT), which transports ADP and ATP across the inner mitochondrial membrane. We investigated whether ANT1 overexpression has protective effects on ischemic hearts. Myocardial infarction was induced in wild-type (WT) and heart-specific ANT1-transgenic (ANT1-TG) rats, and hypoxia was set in isolated cardiomyocytes. ANT1 overexpression reduced the myocardial infarct area and increased the survival rate of infarcted rats. Reduced ANT1 expression and increased 4-hydroxynonenal modification of ANT paralleled to impaired ANT function in infarcted WT hearts. ANT1 overexpression improved ANT expression and function. This was accompanied by reduced mitochondrial cytochrome C release and caspase-3 activation. ANT1-TG hearts suffered less from oxidative stress, as shown by lower protein carbonylation and 4-hydroxynonenal modification of ANT. ANT1 overexpression also increased cell survival of hypoxic cardiomyocytes and attenuated reactive oxygen species (ROS) production. This was linked to higher stability of mitochondrial membrane potential and lower activity of ROS detoxifying catalase. ANT1-TG cardiomyocytes also showed higher resistance against H2O2 treatment, which was independent of catalase activity. In conclusion, ANT1 overexpression compensates impaired ANT activity under oxygen-restricted conditions. It reduces ROS production and oxidative stress, stabilizes mitochondrial integrity, and increases survival, making ANT1 a component in ROS management and heart protection during ischemia. KEY MESSAGES: ANT1 overexpression reduces infarct size and increases survival after infarction. ANT1 overexpression compensates restricted ANT expression and function in infarcted hearts. Increased ANT1 expression enhances mitochondrial integrity. ANT1-overexpressing hearts reduce oxidative stress by decreasing ROS generation. ANT1 is a component in ROS management and heart protection.
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