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The YAP/SERCA2a signaling pathway protects cardiomyocytes against reperfusion-induced apoptosis

Jiankai Zhong1, Haichun Ouyang1, Sulin Zheng1

  • 1Department of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan 528308, Guangdong, China.

Aging
|July 10, 2020
PubMed

Insights

The yes-associated protein (YAP)/sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) pathway protects heart cells from injury. Activating this pathway reduces mitochondrial damage and endoplasmic reticulum stress after ischemia/reperfusion.

Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Mitochondrial Function

Background:

  • Mitochondria and endoplasmic reticulum (ER) contribute to cardiac ischemia/reperfusion (I/R) injury.
  • Overexpression of yes-associated protein (YAP) or sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) can protect cardiomyocytes from I/R injury.

Purpose of the Study:

  • To investigate the role of the YAP/SERCA2a pathway in mitigating cardiac I/R injury.
  • To elucidate the mechanisms by which YAP/SERCA2a activation protects cardiomyocytes.

Main Methods:

  • Investigated the effects of I/R treatment on YAP and SERCA2a expression in cardiomyocytes.
  • Examined the impact of YAP overexpression on SERCA2a transcription and vice versa.
  • Assessed the protective effects of YAP/SERCA2a activation on mitochondrial damage, ER stress (ERS), and cardiomyocyte viability.
  • Utilized gene knockdown of SERCA2a to confirm its role in YAP-mediated protection.

Main Results:

  • I/R injury reduced YAP and SERCA2a expression, decreasing cardiomyocyte viability.
  • YAP overexpression promoted SERCA2a transcription, indicating YAP acts upstream of SERCA2a.
  • YAP/SERCA2a activation preserved mitochondrial redox balance and bioenergetics, suppressed ERS, reduced calcium overload, and inhibited caspase activation.
  • SERCA2a knockdown abolished the protective effects of YAP overexpression.

Conclusions:

  • The YAP/SERCA2a pathway attenuates cardiac I/R injury by reducing mitochondrial damage and ER stress.
  • This pathway maintains cardiomyocyte viability through improved mitochondria-ER communication.
Keywords:
ERI/R injurySERCA2aYAPcardiomyocytesmitochondrial

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