title: Recent advancement of molecular mechanisms of liver fibrosis.
abstract: 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.
authors: Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Blvd, DAVIS, Suite D2099, Los Angeles, CA, 90048, USA. Ekihiro.Seki@cshs.org.
authors: Ekihiro
authors: E
authors: Seki
authors: School of Medicine, University of California San Diego, La Jolla, CA, USA.
authors: David A
authors: DA
authors: Brenner
mesh_terms: D000818:Animals; D001343:Autophagy; D049109:Cell Proliferation; D016922:Cellular Senescence; D016207:Cytokines / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D055166:Hepatic Stellate Cells / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008103:Liver Cirrhosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D058628:Myofibroblasts / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000473:pathology; D012307:Risk Factors; D015398:Signal Transduction
chemical_list: D016207:Cytokines
keywords: Alcoholic liver disease; Angiogenesis; Autophagy; Hepatic stellate cells; IL-17; IL-22; IL-33; Liver cirrhosis; Reversal; Senescence