Last update:
25-Mar-2014

Cirrhosis of the liver is a chronic liver disease characterized by diffuse fibrosis and distortion of the normal nodular architecture of the organ. The pathogenesis of fibrosis in hepatic cirrhosis remains, to a great extent, obscure. The presence of highly vascularized fibrous tissue surrounding the regenerative hepatic nodules suggests that both angiogenic and inflammatory factors are involved in the pathogenesis of the disease. Hepatic stellate cells, which are activated by hypoxia, and a variety of chemokines and cytokines appear to be the key cells at the "crossroads" of communication between angiogenesis, inflammation and fibrosis. Strategically positioned between hepatic and endothelial cells, they are the target and also the source of angiogenic factors and cytokines, and they can finely orchestrate the processes of fibrosis, angiogenesis and inflammation. The endothelium, an organ with great heterogeneity in structure and function and a variety of physiological properties, is involved in the pathogenesis of cirrhosis. Endothelial dysfunction is involved in angiogenesis and inflammation and recently the endothelium has also been linked to the hypercoagulability in cirrhosis which promotes fibrogenesis. This is a review of current concepts of the pathogenesis of cirrhosis and potential for reversal. Endothelial junctions, namely regions of the endothelium with complex structure expressing activation, which had not so far been studied in cirrhosis, are also described.

Key words: Angiogenesis, Cirrhosis, Endothelial marker, Liver, sCD146.