These findings suggest that AMSCs therapy inhibits the TGF-β/Smad2/3 signaling pathway, thereby suppressing myocardial fibrosis in DCM mice.In summary, AMSCs treatment not only reduces collagen deposition and fibrosis but also modulates key fibrotic signaling pathways, highlighting its potential as a therapeutic strategy to combat myocardial fibrosis in diabetic cardiomyopathy. The gene discussed is TGFB1; the disease is familial dilated cardiomyopathy.