[89bio, Inc.] 89bio, Inc. announced positive topline data from the Phase IIb ENLIVEN trial evaluating treatment with pegozafermin in patients with NASH. In the study, both the 44mg Q2W and 30mg QW doses met, with high statistical significance.

[Communications Biology] The expression of myocardial infarction-associated transcript (MIAT) was up-regulated during liver fibrosis. Silencing MIAT led to the suppression of hepatic stellate cell proliferation and collagen expression.

[EMBO Molecular Medicine] WD-repeat 6 (WDR6) deficiency in hepa1-6 cells drastically inhibited the growth and lung metastasis of orthotopically implanted tumors in immune-competent C57BL/6J mice.

[Cell Death & Disease] Researchers reported that glycerol-3-phosphate acyltransferase 3 (GPAT3) played a key role in Kupffer cells (KCs) inflammation response. Their findings indicated that lipopolysaccharide-mediated inflammatory activation markedly increased lipid droplets accumulation in KCs.

[Heliyon] High-throughput RNA-sequencing analysis was conducted to identify the expression profile of circRNAs in HCC tissues and circ_0005218 was identified as one circRNA that significantly up-regulated in early recurrent HCC tissues.

[Hepatology] Investigators examined the role of parathyroid hormone receptor-1 signaling in the activation of hepatic stellate cells and hepatic fibrosis.

[Experimental Cell Research] The authors found that the expression of KIFC3 was upregulated in HCC, and high KIFC3 expression was related to poor overall survival.

[Biotechnology and Genetic Engineering Reviews] Scientists proved that LncRNA MBNL1-AS1 increased the tripterine resistance of HCC cells at least partly by mediating miR-708-5p-related glycolysis.

[Nature Communications] Researchers showed that the secreted pseudo serine protease PRSS35 functions as a tumor suppressor in HCC. Mechanistically, they demonstrated that active PRSS35 was processed via cleavage by proprotein convertases.

[Molecular and Cellular Biochemistry] The authors summarize the recent studies focusing on various components of the lipophagic machinery that can be modulated for their potential role as therapeutic agents against a wide range of liver diseases.

[Hepatology] Scientists describe conserved and distinct pathogenic pathways highlighting therapeutic targets which may be of potential in both alcohol-associated liver disease (ALD) and non-alcoholic fatty liver disease, and those which are unique to each disease.

[Journal Of Clinical Investigation] Researchers showed that RB1-loss/E2F activation sensitized cancer cells to ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, by upregulating expression of ACSL4 and enriching ACSL4-dependent arachidonic acid-containing phospholipids, which are key components of ferroptosis execution.