ArticleJournal of cellular and molecular medicine2011
Mitochondrial cyclophilin-D as a potential therapeutic target for post-myocardial infarction heart failure.
Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- Endogenous complement 1q binding protein (C1qbp) regulates mitochondrial permeability transition and post-myocardial infarction remodeling and dysfunction.Journal of molecular and cellular cardiology · 2024Article
- Identification of necroptosis-related diagnostic biomarkers in coronary heart disease.Heliyon · 2024Article
- The SIRT3-ATAD3A axis regulates MAM dynamics and mitochondrial calcium homeostasis in cardiac hypertrophy.International journal of biological sciences · 2024Article
- Cyclophilin inhibition as a strategy for the treatment of human disease.Frontiers in pharmacology · 2024Review
- Neutrophil extracellular trap is an important connection between hemodialysis and acute myocardial infarction.Renal failure · 2023Article
- Inefficient Batteries in Heart Failure: Metabolic Bottlenecks Disrupting the Mitochondrial Ecosystem.JACC. Basic to translational science · 2022Review
- Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease.Cell death & disease · 2022Review
- 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
- Insight into Crosstalk Between Mitophagy and Apoptosis/Necroptosis: Mechanisms and Clinical Applications in Ischemic Stroke.Current medical science · 2022Review
- RIPK3 Induces Cardiomyocyte Necroptosis via Inhibition of AMPK-Parkin-Mitophagy in Cardiac Remodelling after Myocardial Infarction.Oxidative medicine and cellular longevity · 2021Article
- Article
- Proximal tubule cyclophilin D regulates fatty acid oxidation in cisplatin-induced acute kidney injury.Kidney international · 2020Article
- Cyclophilin D: An Integrator of Mitochondrial Function.Frontiers in physiology · 2020Review
- Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials.British journal of pharmacology · 2019Review
- Targeting Mitochondrial Fission Using Mdivi-1 in A Clinically Relevant Large Animal Model of Acute Myocardial Infarction: A Pilot Study.International journal of molecular sciences · 2019Article
- Autophagy, apoptosis, and mitochondria: molecular integration and physiological relevance in skeletal muscle.American journal of physiology. Cell physiology · 2019Article
- Protective Effect of Right Ventricular Mitochondrial Damage by Cyclosporine A in Monocrotaline-induced Pulmonary Hypertension.Korean circulation journal · 2018Article
- Ripk3 promotes ER stress-induced necroptosis in cardiac IR injury: A mechanism involving calcium overload/XO/ROS/mPTP pathway.Redox biology · 2018Article
- Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases.The Biochemical journal · 2018Review
- Heart failure-induced activation of phospholipase iPLAThe Journal of biological chemistry · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The pharmacological inhibition or genetic ablation of cyclophilin-D (CypD), a critical regulator of the mitochondrial permeability transition pore (mPTP), confers myocardial resistance to acute ischemia-reperfusion injury, but its role in post-myocardial infarction (MI) heart failure is unknown. The aim of this study was to determine whether mitochondrial CypD is also a therapeutic target for the treatment of post-MI heart failure. Wild-type (WT) and CypD(-/-) mice were subjected to either sham surgery or permanent ligation of the left main coronary artery to induce MI, and were assessed at either 2 or 28 days to determine the long-term effects of CypD ablation. After 2 days, myocardial infarct size was smaller and left ventricular (LV) function was better preserved in CypD(-/-) mice compared to WT mice. After 28 days, when compared to WT mice, in the CypD(-/-) mice, mortality was halved, myocardial infarct size was reduced, LV systolic function was better preserved, LV dilatation was attenuated and in the remote non-infarcted myocardium, there was less cardiomyocyte hypertrophy and interstitial fibrosis. Finally, ex vivo fibroblast proliferation was found to be reduced in CypD(-/-) cardiac fibroblasts, and in WT cardiac fibroblasts treated with the known CypD inhibitors, cyclosporin-A and sanglifehrin-A. Following an MI, mice lacking CypD have less mortality, smaller infarct size, better preserved LV systolic function and undergo less adverse LV remodelling. These findings suggest that the inhibition of mitochondrial CypD may be a novel therapeutic treatment strategy for post-MI heart failure.
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Registered trials
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.