SIRT7, a member of the sirtuin family, is an NAD+-dependent lysine deacetylase and deacylase. It plays crucial roles in diverse biological processes, including metabolism, stress responses, and aging [1,2,5]. SIRT7 is involved in pathways such as glucose and lipid metabolism, DNA damage repair, and ribosomal RNA expression [1,2,4]. Genetic models, like KO/CKO mouse models, have been valuable in studying its functions.

In mice, loss of Sirt7 impedes the hair follicle life-cycle transition from telogen to anagen phase, delaying hair growth, while its overexpression accelerates this process. Mechanistically, Sirt7 interacts with and deacetylates Nfatc1, leading to its degradation and promoting anagen entry [3]. In pulmonary hypertension, SIRT7 levels are reduced. Pulmonary endothelium-specific depletion of Sirt7 exacerbates the disease, while its overexpression reverses the phenotypes by deacetylating KLF4 and maintaining pulmonary arterial endothelium cell (PAEC) homeostasis [6].

In conclusion, SIRT7 is essential for processes like hair growth and maintaining PAEC homeostasis. Mouse KO/CKO models have revealed its significance in diseases such as hair growth disorders and pulmonary hypertension, providing insights into potential therapeutic strategies targeting SIRT7 in these conditions.