ArticleBiomedicines2022
Cardioprotection Attributed to Aerobic Exercise-Mediated Inhibition of ALCAT1 and Oxidative Stress-Induced Apoptosis in MI Rats.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Effect of aerobic training on apoptosis biomarkers and cardiac wall stress in healthy and streptozotocin-induced diabetic male rats.American heart journal plus : cardiology research and practice · 2026Article
- Identification of lipid metabolism-related genes in myocardial infarction: implications for diagnosis and therapy.Journal of cardiothoracic surgery · 2025Article
- Molecular Mechanism of Aerobic Exercise Ameliorating Myocardial Mitochondrial Injury in Mice with Heart Failure.International journal of molecular sciences · 2025Article
- High-intensity interval training attenuates renal injury induced by myocardial ischemia-reperfusion in rats.Journal of the Chinese Medical Association : JCMA · 2025Article
- Physical Exercise: A Promising Treatment Against Organ Fibrosis.International journal of molecular sciences · 2025Review
- ALCAT1-Mediated Pathological Cardiolipin Remodeling and PLSCR3-Mediated Cardiolipin Transferring Contribute to LPS-Induced Myocardial Injury.Biomedicines · 2024Article
- Aerobic exercise protects MI heart through miR-133a-3p downregulation of connective tissue growth factor.PloS one · 2024Article
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5 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiolipin (CL) plays a pivotal role in mitochondria-mediated apoptosis. Acyl-CoA: lysocardiolipin acyltransferase 1 (ALCAT1) can accelerate CL reactive oxygen production and cause mitochondrial damage. Although we have demonstrated that aerobic exercise significantly reduced ALCAT1 levels in MI mice, what is the temporal characteristic of ALCAT1 after MI? Little is known. Based on this, the effect of exercise on ALCAT1 in MI rats needs to be further verified. Therefore, this paper aimed to characterize ALCAT1 expression, and investigate the possible impact of exercise on ALCAT1 and its role in fibrosis, antioxidant capacity, and apoptosis in MI rats. Our results indicated that the potential utility of MI increased ALCAT1 expression within 1-6 h of MI, and serum CK and CKMB had significant effects in MI at 24 h, while LDH exerted an effect five days after MI. Furthermore, ALCAT1 expression was upregulated, oxidative capacity and excessive apoptosis were enhanced, and cardiac function was decreased after MI, and aerobic exercise can reverse these changes. These findings revealed a previously unknown endogenous cardiac injury factor, ALCAT1, and demonstrated that ALCAT1 damaged the heart of MI rats, and aerobic exercise reduced ALCAT1 expression, oxidative stress, and apoptosis after MI-induced cardiac injury in rats.
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