ALK1-Smad1/5 signaling pathway in fibrosis development: Friend or foe?
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- 作者：Jos茅 M. Mu帽oz-F茅lix ; Mar铆a Gonz谩lez-N煤帽ez ; Jos茅 M. L贸pez-Novoa
- 关键词：Cirrhosis ; Collagen ; Extracellular matrix ; Fibrosis ; Smad
- 刊名：Cytokine and Growth Factor Reviews
- 出版年：December, 2013
- 年：2013
- 卷：24
- 期：6
- 页码：523-537
- 全文大小：2327 K
文摘
Fibrosis is a common phenomenon associated with several pathologies, characterized by an excessive extracellular matrix deposition that leads to a progressive organ dysfunction. Thus fibrosis has a relevant role in chronic diseases affecting the kidney, the liver, lung, skin (scleroderma) and joints (arthritis), among others. The pathogenesis of fibrosis in different organs share numerous similarities, being one of them the presence of activated fibroblasts, denominated myofibroblast, which act as the main source of extracellular matrix proteins. Transforming growth factor beta-1 (TGF-尾1) is a profibrotic cytokine that plays a pivotal role in fibrosis. The TGF-尾1/ALK5/Smad3 signaling pathway has been studied in fibrosis extensively. However, an increasing number of studies involving the ALK1/Smad1 pathway in the fibrotic process exist. In this review we offer a perspective of the function of ALK1/Smad1 pathway in renal fibrosis, liver fibrosis, scleroderma and osteoarthritis, suggesting this pathway as a powerful therapeutical target. We also propose several strategies to modulate the activity of this pathway and its consequences in the fibrotic process.