Abstract: Diabetic cardiomyopathy (DCM) is a chronic disease characterized by metabolic dysregulation that is often accompanied by local inflammation, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, cardiomyocyte apoptosis, and fibrosis.
No specific drugs have yet been approved for treating DCM, the leading cause of death among people with diabetes.
The pathogenetic mechanisms of DCM are characterized not only by changes in protein levels, but also by their post-translational modifications, which are of utmost importance. One such modification is lysine residue acetylation, which has a crucial role in metabolic homeostasis through the regulation of multiple cellular processes. The deacetylase group of enzymes named sirtuins are key players in controlling reversible acetylation of proteins.
Accumulating evidences suggest that sirtuins play an important role in several of the mechanisms involved in DCM development and progression. Several studies have demonstrated their efficacy in both animal models and humans with DCM and, thus, strategies aimed at modulating sirtuin activity have become of clinical interest.
