Pharmacological inhibition of either Drp1 or ERK1/2 signaling reversed the impairment of ACh-induced relaxation in db/db mice treated with MSCs caused by STC1 knockdown (Fig. S8C, D), whereas there was no significant difference in endothelium-independent relaxation among these groups, indicating that MSCs injection prevent endothelial dysfunction in diabetic mice through STC1-dependent inhibition of mitochondrial fission. This evidence concerns the gene DNM1L and endothelial dysfunction.