The scheme summarises critical aspects of MHN-associated ALF. (IMAGE)

First Hospital of Jilin University

The scheme summarises critical aspects of MHN-associated ALF.

Caption

MHN-associated ALF has unique aetiologies, including HAV, HBV, HEV, AIH and idiosyncratic drugs. Following MHN, HSCs, Mϕs, LSECs, other inflammatory cells (eg, neutrophils, NK cells, T cells and B cells) are activated or recruited, thereby constituting disease microenvironment. One week after disease onset is a ‘golden window’. LPCs are rapidly activated and proliferate following MHN. Whether LPCs rapidly and sufficiently take over hepatocyte functions determines the performance during the golden window and subsequent clinical outcome. Over time, LPCs differentiate into mature hepatocytes, thereby recovering damaged liver architecture. Hepatic master transcription factors (HNF4α, C/EBPα, FOXA2 and FOXA3) play critical roles in LPC activation and transdifferentiation into mature hepatocytes. Created with BioRender.com. AIH, autoimmune hepatitis; ALF, acute liver failure; C/EBP, CCAAT/enhancer binding protein; DR, ductular reaction; FOXA, forkhead box A; HAV, hepatitis A virus; HBV, hepatitis B virus; HC, hepatocyte; HEV, hepatitis E virus; HNF4α, hepatocyte nuclear factor 4α; HSCs, hepatic stellate cells; IHLC, intermediate hepatocyte-like cells; LPCs, liver progenitor cells; LSECs, liver sinusoidal endothelial cells; MHN, massive hepatic necrosis; Mϕs, macrophages; Neu, neutrophils; NK, natural killer.

Credit

By Honglei Weng, Roman Liebe, et al.

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CC BY

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