SIRT3-mediated cardiac remodeling/repair following myocardial infarction

The recent investigations have extensively focused on the importance of sirtuins, as a highly conserved family of
gene products, particularly SIRT3 in various biological and pathological processes. SIRT3, the mitochondrial
NAD+-dependent deacetylase has been demonstrated to target a broad range of proteins involved in the oxidative stress, ischemia–reperfusion injury, mitochondrial metabolism homeostasis and cellular death. The critical function of SIRT3 in myocardial infarction (MI), which is one of the complex phenotype of coronary artery
disease and a result of interaction between various genetic and environmental factors, as well as in cardiac repair
and remodeling post-MI have attracted more attention in the recent years. Therefore, in this review, we will
summarize important literature about the involvement of SIRT3 in cardiac remodeling/repair following MI and
its potential underlying mechanisms