ArticleMolecular medicine (Cambridge, Mass.)2024
Aerobic exercise inhibits GSDME-dependent myocardial cell pyroptosis to protect ischemia-reperfusion injury.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Limonin alleviates pyroptosis and inflammatory responses in cardiomyocytes of myocardial ischemia-reperfusion mice by inhibiting the caspase-3/GSDME pathway.Frontiers in immunology · 2026Article
- Delta opioid peptide (D-Ala2, D-Leu5)-enkephalin (DADLE) mitigates myocardial ischemia-reperfusion injury by inhibiting the TRAF6/NF-κB/NLRP3 pathway.Iranian journal of basic medical sciences · 2026Article
- IGFBP2 plays a key role in aerobic exercise-mediated inhibition of ferroptosis in cardiac ischemia/reperfusion (I/R) injury.Journal of translational medicine · 2025Article
- Kaempferol inhibits cardiomyocyte pyroptosis via promoting O-GlcNAcylation of GSDME and improved acute myocardial infarction.BMC pharmacology & toxicology · 2025Article
- GSDME in cardiovascular diseases: research system and contemporary progress.Frontiers in immunology · 2025Review
- PANoptosis: a potential target of cardiomyopathy.Frontiers in immunology · 2025Review
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundAcute myocardial infarction (AMI) remains a significant cause of global mortality, exacerbated by ischemia-reperfusion (IR) injury. Myocardial cell pyroptosis has emerged as a critical pathway influencing IR injury severity.
methodsWe aimed to investigate the cardioprotective effects of aerobic exercise on IR injury by examining the modulation of IGFBP2 and its impact on GSDME-dependent myocardial cell pyroptosis. Mechanistic pathways were explored using western blot analysis, ELISA, immunofluorescence, and echocardiography.
resultsOur findings demonstrate that aerobic exercise leads to increased circulating levels of IGFBP2, which effectively suppresses GSDME-dependent myocardial cell pyroptosis. This regulation occurs via the AKT-GSK3β signaling pathway, involving VDAC1 phosphorylation, thereby enhancing mitochondrial function and reducing oxidative stress.
conclusionIn conclusion, our study highlights the role of IGFBP2 in mitigating GSDME-dependent pyroptosis as a mechanism through which aerobic exercise exerts cardioprotective effects against IR injury. These insights suggest potential therapeutic targets for managing acute myocardial infarction.
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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 Socratic graph.