HDAC7 (histone deacetylase 7) is a class IIa histone deacetylase that regulates gene transcription through epigenetic mechanisms and cellular localization. HDAC7 deacetylates lysine residues on core histones and non-histone proteins, playing crucial roles in transcriptional repression and cellular differentiation 1. The enzyme exhibits cell-type-specific functions, cooperating with HDAC4 in Th17 cell differentiation by interacting with transcription factors JunB and Aiolos to regulate inflammatory gene expression 1. In cancer, HDAC7 promotes tumorigenesis through multiple mechanisms: it forms a positive feedback loop with β-catenin/c-Myc in esophageal squamous cell carcinoma 2 and drives glioblastoma toward a mesenchymal-like state via LGALS3-mediated crosstalk between cancer cells and macrophages 3. In neurodegeneration, HDAC7 upregulation in astrocytes contributes to Alzheimer's disease pathology by deacetylating transcription factor TFEB at K310, preventing its nuclear translocation and inhibiting lysosomal biogenesis necessary for tau clearance 4. HDAC7 also regulates metabolic processes, with β-hydroxybutyrate inhibiting its activity to facilitate FOXO1 nuclear exclusion and suppress gluconeogenesis 5. Additionally, HDAC7 mediates endothelial-mesenchymal transition in diabetic retinopathy through the FOXO1/ZEB1 axis 6.