ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2018
Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The Role of Estrogen in Mitochondrial Disease.Cellular and molecular neurobiology · 2025Pooled it
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- The role of sirtuins in the regulation of reactive oxygen species in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2025Review
- Cardioprotective effect of Yiqi Huoxue decoction on post-myocardial infarction injury mediated by CaFrontiers in cardiovascular medicine · 2025Article
- Mitochondrial Volume Regulation and Swelling Mechanisms in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Review
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- Salix subserrata Bark Extract-Loaded Chitosan Nanoparticles Attenuate Neurotoxicity Induced by Sodium Arsenate in Rats in Relation with HPLC-PDA-ESI-MS/MS Profile.AAPS PharmSciTech · 2022Article
- Glucogallin Attenuates RAW 264.7 Cells from Arsenic Trioxide Induced Toxicity via the NF-ҡB/NLRP3 Pathway.Molecules (Basel, Switzerland) · 2022Article
- Perspectives on mitochondrial relevance in cardiac ischemia/reperfusion injury.Frontiers in cell and developmental biology · 2022Review
- Review
- Mitochondria as a therapeutic target for cardiac ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2021Review
- Targeting the Mitochondrial Permeability Transition Pore to Prevent Age-Associated Cell Damage and Neurodegeneration.Oxidative medicine and cellular longevity · 2021Review
- Mitochondrial respiratory supercomplexes in mammalian cells: structural versus functional role.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Cardiac Function is not Susceptible to Moderate Disassembly of Mitochondrial Respiratory Supercomplexes.International journal of molecular sciences · 2020Article
- The Role of Reactive Oxygen Species in Arsenic Toxicity.Biomolecules · 2020Review
- The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsThe mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against ischemia-reperfusion injury on various animal models, mostly in males. However, failure of recent clinical trials requires a detailed elucidation of the cardioprotective efficacy of CyP-D inhibition. The aim of this study was to examine whether cardioprotective effects of sanglifehrin A, a potent inhibitor of CyP-D, on post-infarcted hearts depends on reperfusion.
methodsAcute or chronic myocardial infarction was induced by coronary artery ligation with/without subsequent reperfusion for 2 and 28 days in female Sprague-Dawley rats. Cardiac function was estimated by echocardiography. Oxygen consumption rates, ROS production, permeability transition pore opening, protein carbonylation and respiratory supercomplexes were analyzed in isolated cardiac mitochondria.
resultsSanglifehrin A significantly improved cardiac function of reperfused hearts at 2 days but failed to protect after 28 days. No protection was observed in non-reperfused post-infarcted hearts. The respiratory control index of mitochondria was significantly reduced in reperfused infarcted hearts at 2-days with no effect at 28-days post-infarction on reperfused and non-reperfused hearts. Likewise, only a minor increase in reactive oxygen species production was observed at 2-days in non-reperfused post-infarcted hearts.
conclusionThis study demonstrates that CyP-D inhibition exerts cardioprotective effects in reperfused but not in non-reperfused infarcted hearts of female rats, and the effects are observed only during acute post-infarction injury.
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Registered trials
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