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. 2016 Jan 12;5(1):7. doi: 10.3390/jcm5010007

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© 2016 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).

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Liver regeneration-related EMT and phospho-Smad signaling in acute liver disease. (A) Quiescent hepatic stellate cells (HSC) are characterized by retinoid droplets in the cytoplasm. Acute liver injury caused HSC activation and hepatocyte damage, necrosis and EMT. Activated HSC move from the space of Disse to sites of damage where the activated HSC contribute to tissue repair by producing large amounts of collagen. HSC also play an important role in secreting TGF-β. (B) Catalytically-active TβRI phosphorylates COOH-tail serine residues of Smad2 and Smad3. Both pSmad2C and pSmad3C are localized in the nuclei of hepatocytes and mesenchymal cells in acute injured liver. After binding with Smad4, pSmad2/3C translocate with Smad4 to the nucleus and bind to the collagen promoter. pSmad2/3C stimulate extracellular matrix (ECM) deposition and suppress cell growth by c-Myc inhibition. However, Smad7 induced by the pSmad3L/C signal terminates the fibrogenic phospho-Smad signaling. This negative feedback mechanism of the fibrogenic TGF-β/CK signal results in a transient collagen synthesis in the activated HSC, which may thus contribute to tissue repair.