Published online Nov 21, 2017. doi: 10.3748/wjg.v23.i43.7666
Peer-review started: July 24, 2017
First decision: August 28, 2017
Revised: September 13, 2017
Accepted: September 28, 2017
Article in press: September 28, 2017
Published online: November 21, 2017
Cirrhosis develops from liver fibrosis and is the severe pathological stage of all chronic liver injury. Cirrhosis caused by hepatitis B virus and hepatitis C virus infection is especially common. Liver fibrosis and cirrhosis involve excess production of extracellular matrix, which is closely related to liver sinusoidal endothelial cells (LSECs). Damaged LSECs can synthesize transforming growth factor-beta and platelet-derived growth factor, which activate hepatic stellate cells and facilitate the synthesis of extracellular matrix. Herein, we highlight the angiogenic cytokines of LSECs related to liver fibrosis and cirrhosis at different stages and focus on the formation and development of liver fibrosis and cirrhosis. Inhibition of LSEC angiogenesis and antiangiogenic therapy are described in detail. Targeting LSECs has high therapeutic potential for liver diseases. Further understanding of the mechanism of action will provide stronger evidence for the development of anti-LSEC drugs and new directions for diagnosis and treatment of liver diseases.
Core tip: Liver sinusoidal endothelial cells (LSECs) comprise the highest proportion of nonparenchymal cells in the liver. Their fenestrae and basement membrane structure, and high endocytic clearance ability play an indispensable role in the physiology and pathology of the liver. LSECs mainly participate in the regulation of liver pathology, such as hepatitis, liver fibrosis, cirrhosis and liver regeneration, by exerting anti-inflammatory activity, endocytosis, secretion, synthesis of angiogenesis signaling molecules and maintaining the hepatic stellate cell phenotype. It is important to elucidate the mechanism of action of LSECs, which will provide important information for future targeted therapy and clinical diagnosis.