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.
LncRNA-Snhg3 regulates lipid metabolism by affecting chromatin accessibility which indicates that lncRNA-mediated epigenetic modification has a crucial role in the pathology of metabolic dysfunction-associated fatty liver disease.
Pharmacological activation of farnesoid X (FXR) receptor by hammerhead-type agonists induces a novel enhancer RNA, termed Fincor, contributing to the amelioration of nonalcoholic steatohepatitis in mice.
Ablation of the G-protein-coupled receptor C3aR1 specifically on macrophages or Kupffer cells does not alter the course of metabolic dysfunction-associated steatotic liver disease in a dietary mouse model.
Fibroblast growth factor 21 blocks hepatic lipid influx and accumulation, prevents Kupffer cell activation, and inhibits the formation of hepatic lipid- and scar-associated macrophages, thereby likely inhibiting fibrogenesis in nonalcoholic steatohepatitis in humanized APOE*3-Leiden.CETP mice.
MIR20B has a deteriorating effect in NAFLD by suppressing PPARA, and may serve as a therapeutic target for combination therapy with fenofibrate for NAFLD.
Inactivation of SURF4 leads to impaired secretion of PCSK9 and apolipoproteins resulting in low plasma cholesterol without detrimental consequences to the liver.
Feedback mechanisms that contribute to the deactivation of the unfolded protein response lead to the dysregulation of mRNA expression during chronic stress in the liver, including that of the critical endoplasmic reticulum chaperone BiP.
