Abstract
Potential drug mechanism(s) targeting the contractile status of hepatic stellate cells
Highlights
Hepatic stellate cells (HSCs) represent the major cell type involved in liver fibrosis
In normal liver HSCs are in a quiescent state; when the liver is damaged, stellate cells can change into an activated state, characterized by proliferation, contractility, chemotaxis, and secretion of extracellular matrix proteins, such as collagen, which can lead to cirrhosis (Li et al, 2008)
HSCs are considered as “hepatic pericytes,” because they possess protrusions that wrap around the sinusoids and their contraction contribute to the modulation of sinusoidal resistance and blood flow (Soon and Yee, 2008)
Summary
Hepatic stellate cells (HSCs) represent the major cell type involved in liver fibrosis. This evidence underscores the role of agonists that increase HSC contractility in the regulation of hepatic blood flow. The transition from NAFLD to NASH depends on a superimposed inflammatory mechanism, that induces activation of HSC, injury to hepatic microcirculation, venous obstruction, increased production of extracellular matrix, and fibrous septation, (Wanless and Shiota, 2004; Bian and Ma, 2012).
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