Table 2.

Hepatic satellite cells role in different liver disease.

Type of disease	Inducing factors	Mechanism	Ref.
HCC	Hepatitis, Alcoholic liver diseases, and NASH	contribute to the formation of tumor microenvironment favorable for tumor growth Activated HSCs in the tumor stroma continuously produce ECM production of soluble factors favoring tumor growth, such as hepatocyte growth factor and TGF-β production of proangiogenic factors such as vascular endothelial growth factor-A (VEGF-A) and MMP9	(87)
I/R liver injury	Ischemia and reperfusion in liver transplantation, imbalances in pH and electrolytes	interaction of CD4+ T cells with HSCs before entering the hepatic parenchyma induce the expansion of regulatory T cells (Protective)	(88–90)
Immune-induced hepatitis	Concanavalin A (ConA) and LPS	control CD4+ T cell trafficking to liver parenchyma contribution of HSCs to massive production of inflammatory cytokines and chemokines by intra- and extrahepatic immune cells in a paracrine manner	(91–93)
NASH	Increased intestinal permeability	The activation of HSCs by TLR4 (the production of chemokines and the expression of adhesion molecules ICAM-1 and VCAM-1 incensement in the interaction between HSCs and Kupffer cells	(94)
Viral hepatitis	Hepatitis B and C virus	inflammatory and fibrogenic responses by HSCs cell proliferation and nonstructural proteins augment ICAM-1 expression and chemokine production through the NF-κB induction cell migration and activation of several inflammatory pathways in response to CCL21 secreted by activated dendritic cells	(95)

HCC, Hepatocellular carcinoma; ECM, extracellular matrix; HSCs, hepatic stellate cells; MMPs, Matrix metalloproteinase; MSCs, Mesenchymal stromal/stem cells; I/R, Ischemia/reperfusion; NF-kB, Nuclear factor kappa-B; LPS, Lipopolysaccharide; TGF-β, Transforming growth factor-beta; NASH, Non-alcoholic steatohepatitis; TLR, Toll-like receptor.