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Updated: Jul 31, 2025
Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
Published on: May 13, 2016
EZH2 serves as a promising therapeutic target for fibrosis
Qian Zhang1, Ya-Xi Wu1, Xiao-Qian Yu1
1State Key Laboratory of Esophageal Cancer Prevention and Treatment, Key Laboratory of Advanced Pharmaceutical Technology, Ministry of Education of China, School of Pharmaceutical Science and Institute of Pharmaceutical Science, Zhengzhou University, Zhengzhou, Henan 450001, PR China.
Abstract:
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-β1 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-β1/Smads, and TGF-β1/non-Smads with fibrosis and described the research progress of EZH2 inhibitors in the treatment of fibrosis.
Insights
Enhancer of zeste homolog 2 (EZH2) plays a key role in fibrosis development. EZH2 inhibitors show promise for treating fibrosis by targeting EZH2 and its associated TGF-β1 signaling pathways.
Area of Science:
- Epigenetics
- Molecular Biology
- Pathology
Background:
- Fibrosis impairs organ function and can lead to sclerosis, cancer, and death.
- Enhancer of zeste homolog 2 (EZH2) is an epigenetic regulator implicated in fibrosis.
- Transforming growth factor-beta 1 (TGF-β1) is a key pro-fibrotic cytokine linked to EZH2 activity.
Purpose of the Study:
- To review the relationship between EZH2, TGF-β1 signaling, and fibrosis.
- To summarize the therapeutic potential of EZH2 inhibitors in treating fibrosis.
Main Methods:
- Literature review of studies on EZH2, TGF-β1 signaling pathways (Smads and non-Smads), and fibrosis.
- Analysis of research on EZH2 inhibitors' efficacy in various fibrotic conditions.
Main Results:
- EZH2 influences fibrosis through epigenetic gene regulation.
- TGF-β1 signaling, via Smads and non-Smads pathways, interacts with EZH2 in fibrosis.
- EZH2 inhibitors have demonstrated efficacy in preclinical models of fibrosis.
Conclusions:
- EZH2 is a critical mediator in fibrosis pathogenesis.
- Targeting EZH2 and its downstream pathways offers a potential therapeutic strategy for fibrosis.
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