ArticleJournal of translational medicine2023
GSDMD-mediated pyroptosis dominantly promotes left ventricular remodeling and dysfunction in post-myocardial infarction: a comparison across modes of programmed cell death and mitochondrial involvement.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Molecular mechanisms of coronary microembolization-induced MINOCA.Basic research in cardiology · 2026Review
- TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular ZnCirculation · 2026Article
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Bibliometric Trends in Inflammasome‑Driven Pyroptosis and Cardiovascular Disease.Journal of inflammation research · 2026Article
- Pharmacological inhibition of apoptosis, necroptosis, and ferroptosis confers effective cardioprotection in post-myocardial infarction in rats.Scientific reports · 2025Article
- Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025Review
- Therapeutic Potential of Gasdermin D-Mediated Myocardial Pyroptosis in Ischaemic Heart Disease: Expanding the Paradigm From Bench to Clinical Insights.Journal of cellular and molecular medicine · 2025Review
- Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner.Cell death & disease · 2025Article
- Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- The Protective Effect of Melatonin on LPS-Induced Myocardial InjuryCombinatorial chemistry & high throughput screening · 2025Article
- Xin-Fu-Kang oral liquid improves cardiac function and attenuates miR-223-associated NF-κB/NLRP3 pyroptotic signaling in chronic heart failure.Frontiers in pharmacology · 2025Article
- Potential Roles of IPBiomolecules · 2024Review
- Aerobic Exercise Activates AMPK/PGC-1α Pathway, Inhibits Cardiomyocyte Apoptosis Improves Mitochondrial and Infarcted Heart Function.Doklady. Biochemistry and biophysics · 2024Article
- Pyroptosis in health and disease: mechanisms, regulation and clinical perspective.Signal transduction and targeted therapy · 2024Review
- Colchicine ameliorates myocardial injury induced by coronary microembolization through suppressing pyroptosis via the AMPK/SIRT1/NLRP3 signaling pathway.BMC cardiovascular disorders · 2024Article
- The Potential Therapeutic Prospect of PANoptosis in Heart Failure.Journal of inflammation research · 2024Review
- NEDD4 Regulated Pyroptosis Occurred from Co-infection between Influenza A Virus and Streptococcus pneumoniae.Journal of microbiology (Seoul, Korea) · 2023Article
- Maresin1 alleviates liver ischemia/reperfusion injury by reducing liver macrophage pyroptosis.Journal of translational medicine · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial infarction (MI) has recently accounted for more than one-third of global mortality. Multiple molecular pathological pathways, such as oxidative stress, inflammation, and mitochondrial dysfunction, have been recognized as possible mechanisms in the development of MI. Furthermore, different phases of ischemic injury following the progression of MI were also associated with multiple types of programmed cell death (PCDs), including apoptosis, necroptosis, ferroptosis, and pyroptosis. However, it remains unknown whether which types of PCDs play the most dominant role in post-myocardial infarction (post-MI).
methodIn this study, we used a preclinical rat model of MI induced by permanent left anterior descending coronary artery (LAD) ligation (n = 6) or a sham operated rat model (n = 6). After a 5-week experiment, cardiac function and morphology, mitochondrial studies, and molecular signaling analysis of PCDs were determined.
resultsHerein, we demonstrated that post-MI rats had considerably impaired cardiac geometry, increased oxidative stress, myocardial injuries, and subsequently contractile dysfunction. They also exhibited worsened cardiac mitochondrial function and dynamic imbalance. More importantly, we found that post-MI mediated abundant myocardial cell death through multiple PCDs, including apoptosis, necroptosis, and pyroptosis, but not ferroptosis.
conclusionIn this study, we provide the first insights into the mechanism of PCDs by pyroptosis, which is leveraged as the most dominant mode of cell death after MI.
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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.