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Promising small molecule anti-fibrotic agents: Newly developed or repositioned drugs targeting myofibroblast transdifferentiation

肌成纤维细胞 转分化 纤维化 癌症研究 Wnt信号通路 细胞外基质 心脏纤维化 生物 细胞生物学 医学 病理 信号转导 干细胞
作者
Shin Ishikane,Masaki Arioka,Fumi Takahashi‐Yanaga
出处
期刊:Biochemical Pharmacology [Elsevier BV]
卷期号:214: 115663-115663 被引量:7
标识
DOI:10.1016/j.bcp.2023.115663
摘要

Fibrosis occurs in all organs and tissues except the brain, and its progression leads to dysfunction of affected organs. Fibrosis-induced organ dysfunction results from the loss of elasticity, strength, and functionality of tissues due to the extracellular matrix secreted by myofibroblasts that express smooth muscle-type actin as a marker. Myofibroblasts, which play a major role in fibrosis, were once thought to originate exclusively from activated fibroblasts; however, it is now clear that myofibroblasts are diverse in origin, from epithelial cells, endothelial cells, adipocytes, macrophages, and other cells. Fibrosis of vital organs, such as the heart, lungs, kidneys, and liver, is a serious chronic disease that ultimately leads to death. Currently, anti-cancer drugs have made remarkable progress, as evidenced by the development of many molecular-targeted drugs, and are making a significant contribution to improving the prognosis of cancer treatment. However, the development of anti-fibrotic agents, which also play an important role in prognosis, has lagged. In this review, the current knowledge regarding myofibroblasts is summarized, with particular attention given to their origin and transdifferentiation signaling pathways (e.g., TGF-β, Wnt/β-catenin, YAP/TAZ and AMPK signaling pathways). The development of new small molecule anti-fibrotic agents and the repositioning of existing drugs targeting myofibroblast transdifferentiation are discussed.
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