Chitinase 3-like-1 promotes Kupffer cells to recruit platelets, thereby contributing to liver injury, and serves as a therapeutic target in acetaminophen-induced liver injury.

IL6ST (gp130) binding proteins, such as HyperIL6, promote liver regrowth in a STAT3-indpependent manner through competitive inhibition of anti-regenerative IL11 signaling.

HepG2 transmitochondrial cybrids of haplogroup J genome had increased sensitivity to aspects of mitochondrial dysfunction induced by tolcapone and 2-hydroxyflutamide, compared to haplogroup H, thus cybrids provide a practical system to investigate the consequences of mitochondrial genome on drug-induced hepatotoxicity.

Lutheran is a novel marker for classification of bile duct remodeling in distinct liver injury, and an interesting functional molecule for investigating the nature of liver stem/progenitor cells during regeneration.

The gut microbe-derived metabolite trimethylamine (TMA) is elevated in patients with alcohol-associated hepatitis and inhibition of the gut microbial enzymes that produce TMA may serve as a tractable therapeutic strategy for the treatment of ethanol-induced liver injury.

MBOAT7 loss of function in hepatocytes contributes to ethanol-induced liver injury, offering crucial insights into the dysregulated lipid metabolism and impaired autophagy associated with advanced liver disease.

Site-specific phosphorylation of the A-kinase anchoring protein 12 (AKAP12) in hepatic stellate cells modulates its scaffolding function and promotes liver fibrosis.

Mouse genetic approaches show that multiple Wnt endothelial sources orchestrate the spatiotemporal distribution of hepatocyte functions during liver maturation and respecify metabolic zonation during liver repair.

The Yap pathway requires two signals to promote organ growth: a cell intrinsic Hippo signal and a signal induced by injury or inflammation.

Ductular reaction often observed in chronic liver pathologies such as in cystic fibrosis could be due to disruption of a novel complex of β-catenin-NF-κB and CFTR in cholangiocytes, which leads to persistent nuclear translocation of p65 and NF-κB activation.