Hepatic stellate cell (HSC) (HSC)

Hepatic stellate cells (HSCs) are specialized perisinusoidal cells located in the space of Disse in the liver, representing approximately 5-8% of total liver cells (Friedman, 2008). In their quiescent state, they are the primary storage site for retinoids (Vitamin A) in the body. However, in response to chronic liver injury, such as viral hepatitis or non-alcoholic steatohepatitis (NASH), HSCs undergo a phenotypic transformation known as activation into myofibroblast-like cells (Tsuchida & Friedman, 2017). This activation is characterized by increased proliferation and the excessive synthesis of extracellular matrix (ECM) proteins, particularly Type I collagen, which is the central driver of liver fibrosis (Bataller & Brenner, 2005). Therapeutic strategies targeting this process aim to inhibit signaling pathways like TGF-beta and PDGF, or promote the clearance of activated cells to halt or reverse fibrotic progression (Schuppan & Kim, 2013). Drugs like Pirfenidone and Sorafenib have been studied for their ability to modulate these HSC functions and reduce collagen deposition (Shi et al., 2017; Hennenberg et al., 2008).

Other names

Ito cellLipocytePerisinusoidal cellFat-storing cell

Inhibition of TGF-beta signaling, inhibition of PDGF-mediated proliferation, inhibition of LOXL2-mediated collagen crosslinking, and induction of HSC apoptosis or reversion to quiescence (Tsuchida & Friedman, 2017; Schuppan & Kim, 2013).