Theranostics 2020; 10(25):11737-11753. doi:10.7150/thno.47717 This issue Cite
Review
1. Lab of Tissue Engineering, Faculty of Life Sciences, Northwest University, 229 TaiBai North Road, Xi'an 710069, China
2. Provincial Key Laboratory of Biotechnology of Shaanxi, Northwest University, 229 TaiBai North Road, Xi'an 710069, China
3. Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education. Faculty of Life Sciences, Northwest University, 229 Taibai North Road, Xi'an 710069, China
4. Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education. School of Medicine, Northwest University, 229 Taibai North Road, Xi'an 710069, China
*These authors contributed equally to this work.
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.
Keywords: Glycogen synthase kinase-3β, Fibrosis, Signaling pathway, Epithelial-mesenchymal transition, Aging