Xu et al. (2021) demonstrated that HDAC5 expression was upregulated in both diabetic and UUO models. Furthermore, suppression of HDAC5 mitigates the progression of hyperglycemia-driven EMT within renal tubular cells. HDAC5 modulates transforming growth factor β1 (TGF-β1) activity via the PI3K/Akt pathway, thereby promoting renal fibrosis under high-glucose conditions. Here, TGFB1 is linked to renal fibrosis.