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The role of bone morphogenetic proteins in liver fibrosis


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Abstract

Liver fibrosis is featured by excessive accumulation of extracellular matrix (ECM) proteins in the injury liver of diseases, including alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH), cirrhosis, and hepatocellular cancer (HCC). However, there is no current therapy for preventing and reversing liver fibrosis. Transforming growth factor-β1 (TGF-β1) is a key profibrotic gene that drives activation of hepatic stellate cells (HSCs) and their transdifferentiation to myofibroblasts producing ECM proteins. Bone morphogenetic proteins (BMPs) belonging to TGF-β big family play important roles in tissue morphogenesis and homeostasis in the bone, cartilage, muscle, kidney, and blood vessels. Accumulating evidence indicates that BMPs are involved in the development and progression of liver fibrosis and liver regeneration. In this review, we summarize the recent findings of the dual roles of BMPs in liver fibrosis. Strategies have been developed to target these molecules to treat liver fibrosis. However, the efficacy is under expectation. Therefore, better understanding of the underlying mechanisms of BMPs in the progression of liver disease is critically important for improving their therapeutic effect.

Keywords

liver fibrosis, bone morphogenetic proteins, transforming growth factor-?, hepatic stellate cells, therapy, ALD, alcoholic liver disease, ECM, extracellular matrix, NAFLD, non-alcoholic fatty liver disease, HCC, hepatocellular cancer, HSCs, hepatic stellate cells, EMT, epithelial-mesenchymal transition, CNS, central nervous system, BDL, bile duct ligation, MCD, methionine choline-deficient, HF, high-fat

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