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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
Summary
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.
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.
