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J Hepatobiliary Pancreat Sci. 2015 Jul;22(7):512-8. doi: 10.1002/jhbp.245. Epub 2015 Apr 13.

Recent advancement of molecular mechanisms of liver fibrosis.

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Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Blvd, DAVIS, Suite D2099, Los Angeles, CA, 90048, USA.
School of Medicine, University of California San Diego, La Jolla, CA, USA.


Liver fibrosis occurs in response to any etiology of chronic liver injury including hepatitis B and C, alcohol consumption, fatty liver disease, cholestasis, and autoimmune hepatitis. Hepatic stellate cells (HSCs) are the primary source of activated myofibroblasts that produce extracellular matrix (ECM) in the liver. Various inflammatory and fibrogenic pathways contribute to the activation of HSCs. Recent studies also discovered that liver fibrosis is reversible and activated HSCs can revert to quiescent HSCs when causative agents are removed. Although the basic research for liver fibrosis has progressed remarkably, sensitive and specific biomarkers as non-invasive diagnostic tools, and effective anti-fibrotic agents have not been developed yet. This review highlights the recent advances in cellular and molecular mechanisms of liver fibrosis, especially focusing on origin of myofibroblasts, inflammatory signaling, autophagy, cellular senescence, HSC inactivation, angiogenesis, and reversibility of liver fibrosis.


Alcoholic liver disease; Angiogenesis; Autophagy; Hepatic stellate cells; IL-17; IL-22; IL-33; Liver cirrhosis; Reversal; Senescence

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