ArticleBioengineered2021
Aquaporin 4 inhibition alleviates myocardial ischemia-reperfusion injury by restraining cardiomyocyte pyroptosis.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Aquaporin-4 suppresses neuronal pyroptosis after ischemic stroke via the IκBα/NF-κB signaling pathway.Frontiers in immunology · 2026Article
- Cardioprotective effects of hUCMSCs-Exosi-EGR1 MN patch in MI/RI by modulating oxidative stress and mitophagy.Materials today. Bio · 2025Article
- Inhibition of mir-155-5p alleviates cardiomyocyte pyroptosis induced by hypoxia/reoxygenation via targeting SIRT1-mediated activation of the NLRP3 inflammasome.Journal of cardiothoracic surgery · 2025Article
- Review
- Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury.Biomolecules · 2022Review
- PAGln, an Atrial Fibrillation-Linked Gut Microbial Metabolite, Acts as a Promoter of Atrial Myocyte Injury.Biomolecules · 2022Article
- CircSLC7A6 promotes the progression of Wilms' tumor via microRNA-107/ ABL proto-oncogene 2 axis.Bioengineered · 2022Article
- Pyroptosis regulators exert crucial functions in prognosis, progression and immune microenvironment of pancreatic adenocarcinoma: a bioinformatic and in vitro research.Bioengineered · 2022Article
- A Cardioplegic Solution with an Understanding of a Cardiochannelopathy.Antioxidants (Basel, Switzerland) · 2021Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial injury caused by ischemia-reperfusion is the main pathological manifestation of coronary artery disease (CAD), which is characterized by high mortality and morbidity. Thus, there's an urgent need to develop efficacious strategies and elucidate the underlying mechanisms to prevent or alleviate myocardial ischemia-reperfusion injury to improve the clinical outcomes in patients. In this study, we took advantage of a typical myocardial cell line of mice (HL-1) and cultured with or without an aquaporin 4 inhibitor (TGN-20 denoted as AQP4i) under normal conditions (NC), ischemia (IS) and ischemia reperfusion (IR), respectively. The cytomorphology, ultrastructure, cell vitality and expression pattern of apoptotic proteins were verified with scanning electron microscope (SEM), immunofluorescence staining, flow cytometry, quantitative real-time PCR and western-blotting analysis, respectively. HL-1 under IS or IR condition revealed higher expression of Aquaporin 4 (Aqp4) compared to the NC group, whereas showed similarity in cytomorphology and ultrastructure. Aqp4 inhibition was sufficient to improve the apoptotic cells in HL-1 while showed minimal effects to the other cellular vitality. Furthermore, the expression pattern of apoptotic proteins and anti-apoptotic proteins together with proinflammatory factors in HL-1 was effectively rescued by Aqp4i treatment both at the mRNA level and protein level. Ischemia and ischemia reperfusion caused higher expression of Aqp4 and resultant increase of cardiomyocyte pyroptosis. Myocardial ischemia-reperfusion injury of HL-1 was effectively alleviated by Aqp4 and pyroptosis inhibition. Our findings provided new references for myocardial ischemia-reperfusion injury management via targeting Aqp4-mediated pyroptosis of cardiomyocyte.
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