ArticleAging2023
Evaluation of time-dependent phenotypes of myocardial ischemia-reperfusion in mice.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- CircRERE promotes myocardial ischemia/reperfusion injury by increasing UHRF1 mRNA decay through targeting PUM2 to reduce Drp1 promoter methylation.Chinese medical journal · 2026Article
- Dynamic changes in OTULIN and progranulin levels in experimental myocardial infarction and cardiac remodeling.Histochemistry and cell biology · 2026Article
- A therapeutic relay strategy enabled by spatiotemporally programmable nanoplatforms for multilayered cardioprotection against MI/RI.Journal of nanobiotechnology · 2026Article
- Article
- Transient Increase in ATInternational journal of molecular sciences · 2026Article
- TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular ZnCirculation · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- The Immediate Cardiovascular and Mitochondrial Response in Ischemic Cardiogenic Shock.Journal of cardiovascular translational research · 2025Article
- Different types of cell death and their interactions in myocardial ischemia-reperfusion injury.Cell death discovery · 2025Review
- Preconditioning with acteoside ameliorates myocardial ischemia‑reperfusion injury by targeting HSP90AA1 and the PI3K/Akt signaling pathway.Molecular medicine reports · 2025Article
- Cardioprotection Through Pharmacological Activation of Sirtuin 5 in a Murine Model of Acute Myocardial Infarction.Drug design, development and therapy · 2025Article
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundA mouse model of myocardial ischemia-reperfusion (I/R) is widely used to study myocardial ischemia-reperfusion injury (I/RI). However, few studies focus on the direct comparison of the extent of pathological events resulting from variant durations of ischemia and reperfusion process.
methodsA mouse model of I/RI was established by ligation and perfusion of the left anterior descending coronary artery (LAD), and the dynamic changes were recorded by electrocardiogram at different stages of I/R. Subsequently, reperfusion duration was used as a variable to directly compare the phenotypes of different myocardial injury degrees induced by 3 h, 6 h and 24 h reperfusion from myocardial infarct size, myocardial apoptosis, myocardial enzyme, and inflammatory cytokine levels.
resultsAll mice subjected to myocardial I/R surgery showed obvious myocardial infarction, extensive myocardial apoptosis, dynamic changes in serum myocardial enzyme and inflammatory cytokines, at least for the first 24 h of reperfusion. The infarct size and apoptosis rates gradually increased with the extension of reperfusion time. The peaks of serum myocardial enzyme and inflammatory cytokines occurred at 6 h and 3 h of reperfusion, respectively. We also established I/R mice models with 30 and 60 mins of ischemia. After 21 days of remodeling, longer periods of ischemia increased the degree of fibrosis and reduced cardiac function.
conclusionsIn summary, we conclude that reperfusion durations of 3 h, 6 h, and 24 h induces different injury phenotypes in ischemia-reperfusion mouse model. At the same time, the ischemia duration before reperfusion also affects the degree of cardiac remodeling.
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