Corroborating with these findings, JP4-039 was shown to improve basal respiration and reserve capacity of human skin fibroblasts with very long-chain acyl-CoA dehydrogenase (VLCAD) or complex I deficiency [36,37].Together, our findings suggest that reduction in mito-ROS in vascular endothelium may play a significant role in JP4-039-mediated improvement in coronary angiogenesis and recovery of post-MI cardiac function in vivo. The gene discussed is ACADL; the disease is myocardial infarction.