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Updated: Dec 6, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Glycogen synthase kinase-3β: a promising candidate in the fight against fibrosis
Hanxue Zheng1,2,3, Zhi Yang3, Zhenlong Xin3
1Lab of Tissue Engineering, Faculty of Life Sciences, Northwest University, 229 TaiBai North Road, Xi'an 710069, China.
Abstract:
Fibrosis exists in almost all organs/tissues of the human body, plays an important role in the occurrence and development of diseases and is also a hallmark of the aging process. However, there is no effective prevention or therapeutic method for fibrogenesis. As a serine/threonine (Ser/Thr)-protein kinase, glycogen synthase kinase-3β (GSK-3β) is a vital signaling mediator that participates in a variety of biological events and can inhibit extracellular matrix (ECM) accumulation and the epithelial-mesenchymal transition (EMT) process, thereby exerting its protective role against the fibrosis of various organs/tissues, including the heart, lung, liver, and kidney. Moreover, we further present the upstream regulators and downstream effectors of the GSK-3β pathway during fibrosis and comprehensively summarize the roles of GSK-3β in the regulation of fibrosis and provide several potential targets for research. Collectively, the information reviewed here highlights recent advances vital for experimental research and clinical development, illuminating the possibility of GSK-3β as a novel therapeutic target for the management of tissue fibrosis in the future.
Insights
Glycogen synthase kinase-3β (GSK-3β) shows promise in combating fibrosis by inhibiting extracellular matrix accumulation and epithelial-mesenchymal transition. This review explores GSK-3β's role in fibrogenesis, highlighting its potential as a therapeutic target.
Area of Science:
- Biomedical research
- Cellular biology
- Pathology
Background:
- Fibrosis is a significant factor in disease progression and aging, with no current effective treatments.
- Fibrogenesis, the process of fibrosis, impacts nearly all human organs and tissues.
- Glycogen synthase kinase-3β (GSK-3β) is a key signaling mediator in various biological processes.
Purpose of the Study:
- To review the role of GSK-3β in regulating fibrosis across different organs.
- To identify upstream regulators and downstream effectors of the GSK-3β pathway in fibrosis.
- To explore the potential of GSK-3β as a novel therapeutic target for fibrotic diseases.
Main Methods:
- Literature review and synthesis of existing research on GSK-3β and fibrosis.
- Analysis of GSK-3β's involvement in extracellular matrix accumulation.
- Examination of GSK-3β's influence on epithelial-mesenchymal transition (EMT).
Main Results:
- GSK-3β inhibits extracellular matrix (ECM) accumulation and epithelial-mesenchymal transition (EMT).
- GSK-3β demonstrates protective effects against fibrosis in the heart, lung, liver, and kidney.
- The study outlines upstream regulators and downstream effectors of GSK-3β in fibrotic pathways.
Conclusions:
- GSK-3β plays a crucial protective role in mitigating fibrosis.
- Understanding the GSK-3β pathway offers potential therapeutic strategies for fibrotic conditions.
- GSK-3β represents a promising novel target for future anti-fibrotic therapies.
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