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Background <p>Hypoxia/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.</p> Methods <p>An 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.</p> Results <p>In 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.</p> Conclusion <p>Our 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.</p>

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E3 ubiquitin ligase CHIP alleviates H/R-induced myocardial injury by inhibiting pyroptosis

  • 期刊论文

  • 发表日期：

    2025年4月21日

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  • Liying Hong,
  • Shaolin Gong,
  • Qi Zhang,
  • Xiang Wang,
  • Yongnan Fu

摘要

Background

Hypoxia/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.

Methods

An 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.

Results

In 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.

Conclusion

Our 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.