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Melatonin postconditioning attenuates myocardial ischemia/reperfusion injury by activating YAP to decrease

Tian Tian1, Bin Hu2, Xin-Tao Li1

  • 1Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.

European Journal of Pharmacology
|March 30, 2026
PubMed
Summary
This summary is machine-generated.

Melatonin protects the heart from injury after ischemia and reperfusion by activating Yes-associated protein (YAP), preserving mitochondrial structure and reducing cell death. This study highlights YAP as a potential therapeutic target for heart protection.

Keywords:
Dynamic-related protein 1Ischemia/reperfusion injuryMelatoninMitochondrial fissionYes-associated protein

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Myocardial ischemia/reperfusion (I/R) injury is a significant clinical problem.
  • The role of Yes-associated protein (YAP) in melatonin's protective effects against I/R injury remains unclear.
  • Mitochondrial fission is implicated in I/R injury.

Purpose of the Study:

  • To investigate whether YAP regulates melatonin's protective effects against myocardial I/R injury.
  • To explore the role of YAP in mitochondrial fission during I/R injury.

Main Methods:

  • An in vivo rat model of myocardial I/R injury was utilized.
  • Animals were treated with melatonin, YAP agonist (LPA), or YAP antagonist (verteporfin).
  • Measurements included infarct size, cardiac enzymes, histopathology, oxidative stress markers, apoptosis, and protein expression (YAP, DRP1).

Main Results:

  • Melatonin postconditioning reduced infarct size, oxidative stress, and apoptosis in I/R myocardium.
  • Melatonin treatment enhanced YAP nuclear translocation and modulated DRP1 phosphorylation (increased p-DRP1 Ser637, decreased p-DRP1 Ser616).
  • YAP activation with LPA showed protection, while YAP inhibition with verteporfin exacerbated injury and blocked melatonin's benefits.

Conclusions:

  • Melatonin postconditioning confers cardioprotection against I/R injury by activating YAP.
  • YAP activation preserves mitochondrial ultrastructure by attenuating excessive DRP1-mediated fission.
  • YAP activation represents a potential therapeutic target for myocardial I/R injury, though further dose-response studies are needed.