Mechanistically, activation of TRPV1 by capsaicin reduced MAMs-mediated mitochondrial Ca2+ overload and dysfunction by repressing AMPK/FUNDC1-mediated MAMs formation in podocytes, suggesting that decreased MAMs formation in podocytes alleviates mitochondrial Ca2+ overload-induced mitochondrial dysfunction in the settings of diabetes. Here, FUNDC1 is linked to diabetes mellitus.