ArticleCell cycle (Georgetown, Tex.)2020
Sevoflurane attenuates cardiomyocyte apoptosis by mediating the miR-219a/AIM2/TLR4/MyD88 axis in myocardial ischemia/reperfusion injury in mice.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Sevoflurane suppresses circ_SMG6 to inhibit TLR4/mTOR signaling and attenuate myocardial ischemia-reperfusion injury.Molecular biology reports · 2026Article
- cGAS-STING and PANoptosis: Interplay, Underlying Mechanisms, and Therapeutic Targets.Drug design, development and therapy · 2026Review
- The role of absent in melanoma 2 (AIM2) in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Sevoflurane reduces cardiomyocyte injury in a hypoxia/reoxygenation model of cardiomyocytes through the linc01278/miR-134-5pt regulatory axis.BMC pharmacology & toxicology · 2025Article
- Sevoflurane Alleviates Cardiomyocyte Ferroptosis via Ubiquitin-Specific Protease 7/Phosphatase and Tensin Homolog Modulation.Drug design, development and therapy · 2025Article
- Sevoflurane Affects Myocardial Autophagy Levels After Myocardial Ischemia Reperfusion Injury via the microRNA-542-3p/ADAM9 Axis.Cardiovascular toxicology · 2024Article
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Identifying immune cell infiltration and effective diagnostic biomarkers for ischemic stroke using bioinformatics analysis.PloS one · 2024Article
- The function of miRNAs in the immune system's inflammatory reaction to heart failure.Frontiers in cardiovascular medicine · 2024Review
- Ibuprofen Alleviates Acute Pancreatitis- (AP-) Induced Myocardial Injury by Inhibiting AIM2.Computational and mathematical methods in medicine · 2022Article
- Mesenchymal Stem Cell Exosomal miR-146a Mediates the Regulation of the TLR4/MyD88/NF-Computational and mathematical methods in medicine · 2022Article
- The Association of Serum AIM2 Level with the Prediction and Short-Term Prognosis of Coronary Artery Disease.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022Article
- Emerging Roles of Inflammasomes in Cardiovascular Diseases.Frontiers in immunology · 2022Review
- Maslinic Acid Attenuates Ischemia/Reperfusion Injury-Induced Myocardial Inflammation and Apoptosis by Regulating HMGB1-TLR4 Axis.Frontiers in cardiovascular medicine · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is a vital cause of death and disability globally. The primary treatment for diminishing acute myocardial ischemic injury is myocardial reperfusion, which may induce cardiomyocyte death. Our aim is to unravel the mechanism of sevoflurane (Sev) in microRNA-219a (miR-219a)-mediated regulation of absent in melanoma 2 (AIM2) and TLR4/MyD88 pathway during myocardial ischemia/reperfusion (I/R). The area of MI and apoptosis of cardiomyocytes of the developed mouse model were evaluated by TTC staining and TUNEL, respectively. After the determination of miR-219a as our target using microarray analysis, miR-219a atagomiR was used to treat the mouse model. The luciferase assay verified whether miR-219a targeted AIM2, and the miR-219a and AIM2 expression in myocardial tissues was detected by RT-qPCR and Western blot. miR-219a was significantly increased in myocardial tissues from mice treated with Sev, and the area of MI and cardiomyocyte apoptosis were decreased as a consequence. The miR-219a inhibitor reversed the action of Sev. Moreover, overexpression of AIM2 or induction of the TLR4 pathway aggravated myocardial I/R injury alleviated by miR-219a. All in all, the treatment of Sev upregulated miR-219a expression, which blocked the TLR4 pathway by targeting AIM2 and attenuated cardiomyocyte apoptosis in myocardial I/R mouse model.
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