ArticleJournal of cell communication and signaling2019
Targeting necroptotic cell death pathway by high-intensity interval training (HIIT) decreases development of post-ischemic adverse remodelling after myocardial ischemia / reperfusion injury.
Article in Journal of cell communication and signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- FGF21/sirtuin 1 axis mediates the cardioprotective effects of high-intensity interval training against doxorubicin-induced cardiotoxicity by reducing inflammatory and oxidative stress.Experimental physiology · 2026Article
- High-intensity interval training enhanced cardioprotective effects of neuregulin-1 against doxorubicin-induced cardiotoxicity.Scientific reports · 2026Article
- Targeting necroptosis: how does exercise protect against metabolic dysfunction-associated fatty liver disease?Frontiers in physiology · 2026Review
- High intensity interval training and dalteparin attenuate doxorubicin induced cardiac damage and FoxO4 protein level in rats.Scientific reports · 2025Article
- Targeting necroptosis in Alzheimer's disease: can exercise modulate neuronal death?Frontiers in aging neuroscience · 2025Review
- PANoptosis: a potential target of cardiomyopathy.Frontiers in immunology · 2025Review
- Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Review
- Exercise training and experimental myocardial ischemia and reperfusion: A systematic review and meta-analysis.International journal of cardiology. Heart & vasculature · 2023Review
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
- Necroptosis is required for atrial fibrillation and involved in aerobic exercise-conferred cardioprotection.Journal of cellular and molecular medicine · 2021Article
- Amniotic membrane mesenchymal stem cells labeled by iron oxide nanoparticles exert cardioprotective effects against isoproterenol (ISO)-induced myocardial damage by targeting inflammatory MAPK/NF-κB pathway.Drug delivery and translational research · 2021Article
- Ferroptosis Is a Potential Novel Diagnostic and Therapeutic Target for Patients With Cardiomyopathy.Frontiers in cell and developmental biology · 2021Review
- Human mesenchymal stem cells derived from amniotic membrane attenuate isoproterenol (ISO)-induced myocardial injury by targeting apoptosis.Medical journal of the Islamic Republic of Iran · 2021Article
- Targeting the pathways of regulated necrosis: a potential strategy for alleviation of cardio-cerebrovascular injury.Cellular and molecular life sciences : CMLS · 2021Review
- Mitochondrial and mitochondrial-independent pathways of myocardial cell death during ischaemia and reperfusion injury.Journal of cellular and molecular medicine · 2020Review
- Endothelial to Mesenchymal Transition in the Cardiogenesis and Cardiovascular Diseases.Current cardiology reviews · 2020Review
- Redox Epiphospholipidome in Programmed Cell Death Signaling: Catalytic Mechanisms and Regulation.Frontiers in endocrinology · 2020Review
- Guidelines for evaluating myocardial cell death.American journal of physiology. Heart and circulatory physiology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulated necrosis (necroptosis) plays a pivotal role in the extent of cardiomyocyte loss and the development of post-ischemic adverse remodelling and cardiac dysfunction following myocardial I/R injury. Although HIIT has been reported to give rise to cardioprotection against MI, but the detailed knowledge of its molecular targets for treatment of MI is still not available. The LAD of Male Wistar rats was occluded to induce MI for 30 min and reperfusion for eight weeks. We investigated the effect of long-term HIIT for eight weeks on lipid peroxidation, SOD activity and GSH content using ELISA assay. Cardiac function, fibrosis, and infarct size were assessed by echocardiography, Masson's trichrome and Evans Blue/TTC dual staining respectively. The expressions of gene markers of myocardial hypertrophy, fibrosis and key mediators of necroptosis were measured using RT-PCR and western blotting assay respectively. The results indicated that HIIT reduced lipid peroxidation, infarct size and improved endogenous antioxidant system and heart function. Significant decreases in mRNA levels of procollagen α1(I), α1(III), and fibronectin1were observed following HIIT. Moreover, that HIIT significantly decreased the expression of key mediators of necroptosis induced by MI (P < 0.05). There were no significant differences in β-MHC mRNA level in different groups. The findings of study suggest that HIIT might exert cardioprotective effects against post-ischemic adverse remodeling through targeting necroptosis process. Likewise, cardioprotective effects of HIIT in coping with myocardial I/R injury may be associated with RIP1-RIP3-MLKL axis. These findings establish a critical foundation for higher efficiency of exercise-based cardiac rehabilitation post-MI and future research.
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