ArticleFrontiers in immunology2022
Characterization of early myocardial inflammation in ischemia-reperfusion injury.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Article
- Identification MYD88 as a candidate molecule of sodium overload-induced cell death in myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Article
- Nebivolol as a potential adjunct therapy for sepsis-induced cardiac dysfunction: evidence from a rat model.Scientific reports · 2026Article
- Article
- Article
- Systematic Pharmacology Combined With Experimental Validation Reveals the Apoptosis-Related Mechanism of Simiao Yong'an (SMYA) Decoction Against Myocardial Ischemia-Reperfusion Injury.Cardiovascular therapeutics · 2026Article
- Inhibition of Macrophage ARID3A Alleviates Myocardial Ischemia-Reperfusion Injury After Heart Transplantation by Reducing THBS1/CD47 Signaling-Mediated Neutrophil Extracellular Traps Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- sRAGE inhibits myocardial ischemia/reperfusion injuries via regulating Treg cells.Cell & bioscience · 2025Article
- Current research on mitochondria‑associated membranes in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- Article
- Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis.Redox biology · 2025Article
- Myocardial Infarction Injury Is Exacerbated by Nicotine in Vape Aerosol Exposure.Journal of the American Heart Association · 2025Article
- The role of gut microbiota in myocardial ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2025Review
- Combination of iLux Photothermal Pulsation Therapy with 0.05% Cyclosporine in the Treatment of Meibomian Gland Dysfunction: A Clinical Study.International journal of general medicine · 2025Article
- Recent advancements and comprehensive analyses of butyric acid in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Association between Systemic Immune-Inflammation Index (SII) and New-Onset In-Hospital Heart Failure in Patients with STEMI after Primary PCI.Reviews in cardiovascular medicine · 2024Article
- Construction of a Novel Mitochondria-Associated Gene Model for Assessing ESCC Immune Microenvironment and Predicting Survival.Journal of microbiology and biotechnology · 2024Article
- Curcumin reduces myocardial ischemia-reperfusion injury, by increasing endogenous HMolecular biology reports · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Myocardial injury may be caused by myocardial ischemia-reperfusion (IR), and salvaging such an injury is still a great challenge in clinical practice. This study comprehensively characterized the physiopathologic changes of myocardial injury after IR to explore the underlying mechanism in the early reperfusion phase with particular emphasis on early myocardial inflammation. Methods and Results: The experimental IR model was obtained by the left anterior descending artery's transient ligation of C57BL/6 mice. T2W signals of all mice showed increased signal at different IR stages. It was positively correlated with inflammatory cytokines and cells. T2W imaging by 7.0 T MRI surprisingly detected signal enhancement, but histopathology and flow cytometry did not reveal any inflammatory cells infiltration within 3 h after IR. Cardiomyocyte swelling and increased vascular permeability were observed by WGA staining and ultrastructural analysis, respectively. The 3 h IR group showed that the cardiomyocytes were severely affected with disintegrating myofilaments and mitochondria. Both VEGF and phosphorylated Src protein were markedly expressed in the 3 h IR group in comparison with the sham group, and TUNEL staining displayed little positive cells. Cleaved caspase-3 apoptin also has similar expression levels with that of the sham group. Resident macrophages had notably become M1 phenotype. The T2W signal was still elevated, and we observed that collagen deposition occurred from 1 to 7 days. Conclusions: The inflammation response during the first week after reperfusion injury gradually increase 3 h later, but the main manifestation before that was edema. This study indicated that the first 3 h may be crucial to the early rescue process for reperfusion-induced myocardial injury due to inflammatory cell infiltration absence and apoptosis.
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