Fig. 5

Graphic abstract. Long-term diabetes status (in vivo) and high-glucose microenvironment (in vitro) led to the activation and proliferation of cardiac fibroblasts and subsequently increased the synthesis and secretion of TGF-β, Collagen I and Collagen III, triggering the collagen accumulation and deposition among cardiomyocytes and around vessels, which cause myocardial fibrosis. Lasting cardiac fibrosis without effective intervention induced irreversible injury of cardiac structure and function, resulting in diabetic cardiomyopathy. However, adipose-derived MSC infusion could ameliorate the proliferation and collagen secretion of cardiac fibroblasts caused by high glucose. The underlying mechanism might involve the COX-2 enzyme-mediated arachidonic acid metabolism to release cytokine PGE2 by MSCs under a high-glucose microenvironment. Consequently, MSCs might alleviate myocardial fibrosis and ameliorate abnormal cardiac structure and function of DCM via the COX-2-PGE2 pathway