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

Antibody-mediated neutralisation of Gremlin-1 was ineffective in treating fibrosis in metabolic dysfunction-associated steatohepatitits, likely due to low hepatic expression in a subset of myofibroblasts and redundant Gremlin-1 signalling.

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.

A meta-analysis of single-cell data reveals an advanced and conserved polarisation state of SPP1⁺ macrophages in multiple human fibrotic tissues.

Inhibiting IRE1α decreases tumor cell proliferation and migration in hepatocellular carcinoma, therefore components of this ER-stress pathway may be therapeutically relevant for liver cancer.

Stellate cell lactate transporter MCT1 significantly contributes to liver fibrosis through increased collagen 1 protein expression in vitro and in vivo.

A high-throughput small molecule screen defined compounds that inactivate primary human hepatic stellate cells (HSCs) and led to the identification of nanchangmycin, which regulates intracellular Ca²⁺ levels and the activity of multiple kinases to control HSC fibrotic activity.

Computational and experimental analyses show that homoharringtonine may be repurposed as an agent for the treatment and prevention of liver cancer.

Loss of function of membrane-bound O-acyltransferase 7 (MBOAT7), but not transmembrane channel-like 4 (TMC4), promotes hepatic steatosis.