EZH2 serves as a promising therapeutic target for fibrosis

Fibrosis affects the function of many organs and tissues, and its persistent development can lead to tissue sclerosis and cancer, even leading to death further. Recent studies suggested that enhancer of zeste homolog 2 (EZH2), a major regulator of epigenetic repression, played an important role in the occurrence and development of fibrosis through gene silencing or transcriptional activation. As the most studied and powerful pro-fibrotic cytokine closely related to EZH2, TGF-81 was primarily involved in the regulation of fibrosis along with the typical Smads and non-Smads signaling pathways. In addition, EZH2 inhibitors demonstrated inhibitory effects in several types of fibrosis. This review summarized the relationship underlying the action of EZH2, TGF-81/Smads, and TGF-81/ non-Smads with fibrosis and described the research progress of EZH2 inhibitors in the treatment of fibrosis.

Automated summary

Fibrosis can have detrimental effects on organs and tissues, potentially leading to tissue sclerosis, cancer, and even death. Recent studies have highlighted the role of enhancer of zeste homolog 2 (EZH2), a major regulator of epigenetic repression, in the development of fibrosis through gene silencing or transcriptional activation. Transforming growth factor beta 1 (TGF-β1) has emerged as a key pro-fibrotic cytokine closely associated with EZH2, and it regulates fibrosis through both the classic Smads and non-Smads signaling pathways. EZH2 inhibitors have shown promise in inhibiting fibrosis in various types. This review provides an overview of the interplay between EZH2, TGF-β1/Smads, TGF-β1/non-Smads, and fibrosis, as well as the research progress of EZH2 inhibitors in fibrosis treatment.