New insights into TGF-β/Smad signaling in tissue fibrosis

Publication date: Available online 11 July 2018Source: Chemico-Biological InteractionsAuthor(s): He-He Hu, Dan-Qian Chen, Yan-Ni Wang, Ya-Long Feng, Gang Cao, Nosratola D. Vaziri, Ying-Yong ZhaoAbstractTransforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. This review presents an overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis, followed by an in-depth discussion of their molecular mechanisms of intervention effects both in vitro and in vivo. The role of TGF-β/Smad signaling pathway in tumor or cancer is also discussed. Additionally, the current advances also highlight targeting TGF-β/Smad signaling pathway for the prevention of tissue fibrosis. The review reveals comprehensive pathophysiolog...
Source: Chemico Biological Interactions - Category: Biochemistry Source Type: research

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Source: Mikrobiyoloji Bulteni - Category: Microbiology Tags: Mikrobiyol Bul Source Type: research
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Source: Mikrobiyoloji Bulteni - Category: Microbiology Tags: Mikrobiyol Bul Source Type: research
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