Published online May 27, 2019. doi: 10.4254/wjh.v11.i5.412
Peer-review started: February 25, 2019
First decision: April 22, 2019
Revised: May 14, 2019
Accepted: May 21, 2019
Article in press: May 21, 2019
Published online: May 27, 2019
Processing time: 94 Days and 4.4 Hours
Acute liver failure (ALF) usually results in hepatocellular dysfunction and coagulopathy and carries a high mortality rate. Hepatic stellate cells (HSCs) are famous for their role in liver fibrosis. Although some recent studies revealed that HSCs might participate in the pathogenesis of ALF, the accurate mechanism is still not fully understood. This review focuses on the recent advances in understanding the functions of HSCs in ALF and revealed both protective and promotive roles during the pathogenesis of ALF: HSC activation participates in the maintenance of cell attachment and the architecture of liver tissue via extracellular matrix production and assists liver regeneration by producing growth factors; and HSC inflammation plays a role in relaying inflammation signaling from sinusoids to parenchyma via secretion of inflammatory cytokines. A better understanding of roles of HSCs in the pathogenesis of ALF may lead to improvements and novel strategies for treating ALF patients.
Core tip: Acute liver failure (ALF) is a rare life-threatening disease with a high mortality rate and is characterized by massive hepatocyte death and overactivation of hepatic inflammation. Hepatic stellate cells (HSCs) play both protective and promotive roles during the pathogenesis of ALF: HSC activation participates in the maintenance of cell attachment and the architecture of liver tissue via extracellular matrix production and assists liver regeneration by producing growth factors; and HSC inflammation plays a role in relaying inflammation signaling from sinusoids to parenchyma via secretion of inflammatory cytokines. A better understanding of roles of HSCs in ALF will lead to improvements for treating ALF patients.