• CDC5L is upregulated in post-ischemia-reperfusion myocardium and its overexpression enhances cardiomyocyte proliferation, reduces apoptosis, and improves cardiac function.
• Transcriptomic analysis identifies FGF10 as a key downstream effector of CDC5L, and FGF10 knockdown reverses CDC5L's proliferative and anti-apoptotic effects.
• The cardioprotective effect of CDC5L is mediated through the FGF10-YAP axis, as CDC5L reduces YAP phosphorylation in an FGF10-dependent manner.
• The CDC5L-FGF10-YAP axis offers a promising therapeutic target for promoting myocardial regeneration and recovery after myocardial infarction.