Editorial: SIRT Family in Endocrinology

Tian Li, Fan Peng, Russel J. Reiter, Yang Yang
2019 Frontiers in Endocrinology  
Editorial on the Research Topic SIRT Family in Endocrinology Silent information regulator (SIRT), also known as NAD-dependent deacetylase sirtuin, is a member of the class III group of histone deacetylases, collectively called sirtuins. The mammalian sirtuin family consists of 7 members, designated SIRT1 through SIRT7, which are characterized by a conserved 275-amino-acid catalytic core and unique additional N-terminal and C-terminal sequences of variable length. Previous studies have
more » ... dies have demonstrated that SIRT can deacetylate a range of transcription factors, including forkhead box O (FOXO) transcription factors, p53, nuclear factor-κB (NF-κB), liver X receptor (LXR), peroxisome proliferator-activated receptor γcoactivator-1α(PGC-1α), cAMP-responsive element-binding protein-regulated transcription coactivator 2, and period homolog 2 (1). It has been reported that SIRT performs a wide variety of functions in human systems, including obesity-associated metabolic diseases, endocrine disease, cancer, and aging. Activated SIRT1 improves the insulin sensitivity of liver, skeletal muscle, and adipose tissues and maintains the homeostasis of function and cell mass among pancreatic β-cells, suggesting that SIRT1 might be a new therapeutic target for the prevention of insulin resistance related disease, e.g., metabolic syndrome and type 2 diabetes mellitus (2). In addition, adipose triglyceride lipase (ATGL)mediated SIRT1 activation promotes autophagy/lipophagy as a primary mean to control hepatic lipid droplet (LD) catabolism and fatty acid (FA) oxidation (3). In mammals, SIRT1 can deacetylate and thereby deactivate the p53 protein. SIRT1 also stimulates autophagy by preventing acetylation of proteins (via deacetylation) required for autophagy as demonstrated in cultured cells, embryonic, and neonatal tissues, which provides a link between sirtuin expression and the cellular response to limited nutrients due to caloric restriction (4). Furthermore, SIRT1 is shown to deacetylate and affect the activity of both members of the PGC1-alpha/ERR-alpha complex, which are essential to metabolic regulatory transcription factors (5). The research topic covers the themes of diabetes, thyroid diseases, cardiovascular metabolism, cancer endocrinology, bone metabolism. Liu et al. found that estrogen 17β-estradiol (E2) induces CD34 and downregulates SIRT1 in primary mouse airway smooth muscle cells (ASMCs). Then they showed that loss of CD34 inhibits E2-induced reduction of SIRT1 and its enzymatic activity (measured by p53 deacetylation), demonstrating that E2 downregulates SIRT1 through
doi:10.3389/fendo.2019.00347 fatcat:6qqr7k5rqbdsxoddhknmekmsmq