Abstract
Enhancer of zeste homolog 2 (EZH2) is a histone-lysine N-methyltransferase enzyme that catalyzes the addition of methyl groups to histone H3 at lysine 27, leading to gene silencing. Mutation or over-expression of EZH2 has been linked to many cancers including renal carcinoma. Recent studies have shown that EZH2 expression and activity are also increased in several animal models of kidney injury, such as acute kidney injury (AKI), renal fibrosis, diabetic nephropathy, lupus nephritis (LN), and renal transplantation rejection. The pharmacological and/or genetic inhibition of EZH2 can alleviate AKI, renal fibrosis, and LN, but potentiate podocyte injury in animal models, suggesting that the functional role of EZH2 varies with renal cell type and disease model. In this article, we summarize the role of EZH2 in the pathology of renal injury and relevant mechanisms and highlight EZH2 as a potential therapeutic target for kidney diseases.
Highlights
Epigenetics refers to the heritable change of gene function and phenotype without alteration in a genes DNA sequence (Berger et al, 2009)
Studies have shown that Enhancer of zeste homolog 2 (EZH2) inhibition can effectively suppress the development of liver fibrosis (Zeybel et al, 2017), skin fibrosis (Tsou et al, 2019), atrial fibrosis (Song et al, 2019), pulmonary fibrosis (Xiao et al, 2016), and peritoneal fibrosis (Shi et al, 2020). These results suggest that EZH2 may serve as a promising therapeutic target for the treatment of fibrosis in many organ systems
Enhancer of zeste homolog 2 is highly expressed in renal tumors and many kidney diseases
Summary
Epigenetics refers to the heritable change of gene function and phenotype without alteration in a genes DNA sequence (Berger et al, 2009). In vitro and in vivo studies confirmed that the abnormal increase of EZH2 can inhibit the expression level of E-cadherin, induce the epithelial stromal transformation of renal cancer cells, and promote the occurrence, development and recurrence of renal cancer. Both in vitro and in vivo, cisplatin-induced renal tubular cell damage was accompanied by up-regulation of H3K27me3, while 3-DZNep treatment did not affect its expression (Ni et al, 2019).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
