SIRT7, a member of the sirtuin family of NAD+-dependent protein deacetylases, is involved in diverse biological processes. It plays crucial roles in regulating glucose and lipid metabolism by modulating target proteins in adipose and liver tissues [1]. SIRT7 also serves functions like promoting ribosomal RNA expression, aiding DNA damage repair, and regulating chromatin compaction, which are closely related to the aging process [2].

In mice, Sirt7 loss impedes the transition of the hair follicle life-cycle from telogen to anagen phase, delaying hair growth. Conversely, its overexpression during telogen facilitates anagen entry and accelerates hair growth. Mechanistically, Sirt7 interacts with and deacetylates Nfatc1, causing its degradation to promote anagen entry [3]. In the context of melanoma, SIRT7 deficiency potentiates tumor cell death under stress in vitro and suppresses melanoma growth in vivo, as SIRT7 promotes tumor cell survival and immune evasion via the activation of the unfolded protein response [4]. In pancreatic cancer, SIRT7 expression is upregulated, and its O-GlcNAcylation promotes tumor progression by stabilizing the protein and repressing tumour suppressor genes [5]. In pulmonary hypertension, pulmonary endothelium-specific depletion of Sirt7 exacerbates the disease, while its overexpression or activation reverses the phenotypes, as SIRT7 deacetylates KLF4 to maintain pulmonary arterial endothelium cell homeostasis [6].

In summary, SIRT7 is essential for multiple biological processes such as metabolism, hair growth, and cellular stress responses. The use of Sirt7 KO/CKO mouse models has revealed its significant roles in diseases like melanoma, pancreatic cancer, and pulmonary hypertension, providing potential therapeutic targets for these conditions.