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Liver fibrosis develops as a result of an excessive accumulation of extracellular matrix mostly in the context of chronic liver injury. The progression of liver fibrosis may lead to the development of cirrhosis and eventually hepatocellular carcinoma. Only in recent years has angiogenesis been considered as a concomitant process along the progression of liver fibrosis.1 Moreover, angiogenesis has been shown to be of key importance during the development, growth and progression of hepatocellular carcinoma, one of the most vascularised tumours. However, whether angiogenesis determines the progression of liver fibrosis or is merely a consequence of fibrosis progression is still unclear.
The progression from early stages of fibrosis to cirrhosis is by definition, accompanied by structural and anatomical changes in the liver affecting liver perfusion and compromising oxygen supply. Moreover, deposition of extracellular matrix at the space of Disse prevents oxygen diffusion and promotes sinusoidal capillarisation.
But not only structural changes are behind the increased vascularisation in chronic liver diseases. Activation of hepatic stellate cells, endothelial dysfunction and recruitment of inflammatory cells determine the production of pro-angiogenic factors and a misbalance in the synthesis of vasoactive and inflammatory substances, creating a pro-angiogenic milieu.1
The mechanisms linking inflammation, fibrosis and angiogenesis have not yet been identified and remain an open field that will certainly provide new targets for the treatment of chronic liver diseases. Upon …
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