Sirt1, also known as silent information regulator sirtuin 1 or silencing information regulator 2 related enzyme 1, is a highly conserved NAD+-dependent deacetylase belonging to the sirtuin family [1,2]. It is a post-translational regulator that modulates multiple biological processes, such as inflammation, aging, mitochondrial biogenesis, autophagy, and cell metabolism, by deacetylating a variety of histone and non-histone proteins [1-3,7-9]. Genetic models, especially gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable tools for studying Sirt1's functions in vivo.

In aging-related studies, Sirt1 expression decreases with aging in mice, and increased Sirt1 expression can extend lifespan in yeast, C. elegans, and mice, suggesting its role in the aging process [2]. In the context of inflammation, alterations in Sirt1 expression and activity are linked to inflammatory diseases [1]. In myocardial ischemia-reperfusion injury, Sirt1 is involved in regulating autophagy, which is a double-edged sword in this injury. Sirt1-mediated autophagy plays different roles at different stages of injury, and targeting this mechanism can develop new drugs [3]. In endocrine disorders, dysregulation in Sirt1-mediated autophagy contributes to the onset and progression of diseases like obesity, type-2 diabetes mellitus, etc. [4].

In conclusion, Sirt1 is a key regulator in multiple biological processes. Model-based research, especially KO/CKO mouse models, has revealed its crucial roles in aging, inflammation, myocardial ischemia-reperfusion, and endocrine disorders. Understanding Sirt1's functions provides potential therapeutic targets for these related diseases.