ACTA1 and renal fibrosis: Since the vicinity of the KLF15 promoter may contain AP-2α binding sites, the formation of the HDAC11- AP-2α complex inhibits KLF15 mRNA and protein levels, and the expression of collagen I, α-SMA, and other genes was increased, thus promoting the progression of renal fibrosis (Mao et al., 2020).