ArticleMolecular biology reports2025
E3 ubiquitin ligase CHIP alleviates H/R-induced myocardial injury by inhibiting pyroptosis.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHypoxia/Reoxygenation (H/R) injury to cardiomyocytes has adverse effects on the function, structure and prognosis of the heart. Studies have shown that H/R injury is closely related to pyroptosis. The inflammatory response induced by pyroptosis, leading to the death of cardiomyocytes. However, the specific mechanism of pyroptosis in myocardial H/R injury is not fully understood. In recent years, the important role of CHIP proteins in cardiovascular diseases has gradually attracted attention. Studies have found that CHIP protein can play an important role in the regulation of pyroptosis. However, its role in ameliorating H/R injury in cardiomyocytes has not been fully studied.
methodsAn in vitro H/R model was constructed, and CHIP was knockdown and overexpression interfered simultaneously. The effect of CHIP on pyroptosis and its reduction of H/R-induced myocardial injury were verified by detection of cell viability, LDH, cell membrane integrity, ROS production, inflammatory factors (NLRP3, Caspase-1, ASC, IL-1β) and β-catenin/HSF1 signaling pathway.
resultsIn our study, we verified that the occurrence of oxidative stress and pyroptosis as well as cell damage was significantly increased in cardiomyocytes after H/R stimulation in vitro. After CHIP knockdown, pyroptosis of cardiomyocytes was further aggravated, accompanied by the down-regulation of HSF1/β-catenin signaling axis. These adverse changes were ameliorated after CHIP overexpression.
conclusionOur study confirmed that CHIP can alleviate H/R-induced myocardial injury by mediating pyroptosis, which may be achieved by regulating HSF1/β-catenin signaling pathway.
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