We have shown that: (a) Sirt3 is essential for apelin-induced angiogenesis in response to ischemia in diabetes;9 (b) loss of Sirt3 limits apelin-overexpression bone marrow cell-mediated angiogenesis and cardiac repair;12 and (c) upregulation of Sirt3 by overexpression of apelin ameliorates diabetic cardiomyopathy in diabetic db/db mice.14 In this study, we further demonstrated that apelin overexpression increases autophagy and reduces NADPH oxidase derived ROS formation in the ischemic hearts of diabetes. The gene discussed is FMO5; the disease is diabetic cardiomyopathy.