Sirt1 and osteoarthritis. Comments on the paper by Gabay et al.: 'Sirt1-deficient mice exhibit an altered cartilage phenotype', Joint Bone Spine 2013

摘要

We read with interest the paper of Gabay et al. [1], demonstrating that Sirtl total body KO mice presented altered cartilage phenotype, with elevated chondrocyte apoptosis and a degrada-tive cartilage process. These results are in line with previous data from the same group [2], and from other teams [3] and confirm the potential implication and interest of Sirtl in osteoarthritis (OA). Sirtl is a class HI histone deacetylase acting as an epigenetic regulator of many physiological processes. These data bring new insight into the epigenetic control of osteoarthritis [4]. Sirtl activity upon cartilage homeostasis may be related to apoptosis regulation [5], but also to regulation of pro-inflammatory cytokine production, particularly TNF, in chondrocytes [6].