HDAC9, a histone deacetylase enzyme belonging to the class IIa of HDACs, catalyzes histone deacetylation. It inhibits cell proliferation through DNA repair, cell cycle arrest, apoptosis induction, and genetic expression alteration. HDAC9 is involved in multiple biological processes and is associated with various pathways related to diseases like atherosclerosis, kidney fibrosis, and intervertebral disc degeneration [4].

In atherosclerosis, reducing HDAC9 protein in animal and cellular models is associated with reduced disease, suggesting HDAC9 inhibition could be a novel treatment approach [1]. In male mice, tubule-specific deletion of HDAC9 or its pharmacological inhibition alleviates epithelial cell cycle arrest in G2/M, reducing kidney fibrosis [2]. HDAC9 knockout mice spontaneously develop age-related intervertebral disc degeneration, while overexpression of HDAC9 in nucleus pulposus cells alleviates the symptoms in a mouse model [3].

In conclusion, HDAC9 plays crucial roles in multiple biological processes and disease conditions. The use of gene knockout mouse models has revealed its significance in atherosclerosis, kidney fibrosis, and intervertebral disc degeneration, providing potential therapeutic targets for these diseases.