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Liver sinusoidal endothelial cells (LSECs) display a unique phenotype and function as the exchange vessels of the liver.1 ,2 When successful, LSECs serve as the most powerful scavenger system in the body, however, during capillarisation (which induces a change in the phenotype of LSECs to a vascular type—vasculogenesis) defenestration and the formation of an organised basement membrane occur, resulting in unhealthy LSECs.2 Capillarisation is an event that precedes most liver diseases such as fibrosis, hepatitis and alcoholic liver injury as well as increases naturally with age (pseudocapillarisation).2
Hedgehog (Hh) signalling is an important component in the regulation of vasculogenesis, which increases during liver injury and influences the function of liver cells including cholangiocytes, hepatocytes, hepatic stellate cells (HSCs) and LSECs.3 ,4 LSECs produce Hh ligands and during vascular development Hh ligands (Sonic hedgehog, Indian hedgehog and Desert hedgehog) are activated, thus influencing the transmembrane receptor Patched which prevents the repression of Smoothened (SMO).3 ,5 This process affects the Gli family of transcription factors (Gli1, Gli2, Gli3) which regulates the transcription of the Hh genes.3 ,5 This autocrine mechanism influences cell viability, production and differentiation. …
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