MTOR and Myocardial fibrosis: Anti-fibrotic and cardiometabolic effects: In diabetic hearts, EGCG improved left ventricular contractile function and reduced hypertrophy (lower heart weight index) and injury markers. It significantly alleviated myocardial fibrosis (less collagen I/III deposition, lower hydroxyproline) by downregulating pro-fibrotic TGF-β1 and MMP-2/9 levels. Notably, EGCG activated cardiac autophagy—increased LC3 and Beclin1—via AMPK upregulation and mTOR inhibition, which in turn repressed the TGF-β/MMP fibrotic pathway.