Quercetin has demonstrated the ability to enhance cardiac function and reduce myocardial fibrosis in animal models of heart failure and myocardial fibrosis by improving mitochondrial energy metabolism and modulating mitochondrial fusion/fission and biosynthesis; however, cell survival was affected as it encouraged SIRT5 expression to desuccinylate IDH2, and si-SIRT5 treatment eliminated quercetin’s protective impact on cellular survival (Chang et al., 2021b). Here, SIRT5 is linked to heart failure.