PINK1 modulates Prdx2 to reduce lipotoxicity-induced apoptosis and attenuate cardiac dysfunction in heart failure mice with a preserved ejection fraction

Abstract

	•Our investigation discloses a pivotal relationship between PINK1 and Prdx2 in the context of HFpEF.
	•Notably, PINK1, in addition to its role in mitochondrial autophagy, can increase Prdx2 expression, effectively remove ROS and attenuate cardiomyocyte apoptosis by modulating the JNK and p38 pathways, thereby alleviating myocardial lipotoxicity and improving HFpEF cardiac function.
	•Our studies offer valuable insights, opening avenues for the development of innovative therapeutic strategies in the prevention and treatment of HFpEF.

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2025 The Author(s). Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.