Liver Disease Diagnosis and Treatment

This study develops a diet-induced MASLD/MASH mouse model showing sex- and PPARγ-dependent effects on liver fibrosis and methionine metabolism.

This study identifies 39 candidate genes involved in MASLD progression using multi-omics and multi-trait analysis, validated through experimental models and an interactive web portal.

This study models the MTARC1 A165T variant in human liver organoids, showing reduced steatosis, inflammation, and fibrosis compared to reference sequence organoids.

This study shows that the BSH inhibitor GR-7 reduces steatosis, inflammation, and fibrosis in a mouse model of MASH through bile acid metabolism reprogramming and immune modulation.

This study compares metabolic responses of primary human hepatocytes and Huh7 cells cultured in physiologically-relevant fatty acid mixtures, finding similar lipid composition and metabolic profiles despite differences in viability and gene expression.

This study shows that myeloid HDAC7 promotes liver inflammation and glucose dysregulation in obesity, using mouse models and human data.

This study examines metabolomic, lipidomic, and enterohormone changes during progression from MASLD to MASH in mice, identifying cholic acid elevation and altered enteroendocrine hormone levels.

This study identifies hyperactivated glycolysis as a driver of spatially-patterned Kupffer cell depletion in MASLD, suggesting glucose metabolism as a therapeutic target.

This study demonstrates that a vascularized liver acinus microphysiological system recapitulates key features of MASLD progression and lipid-induced hepatic insulin resistance.

This study identifies CD4+ T cells as drivers of fibrosis in MASH by showing their proinflammatory activity and the therapeutic potential of targeting the OX40L-OX40 axis.

This study identifies molecular changes in early MASLD progression in obesity through transcriptomic and metabolomic analyses, revealing distinct metabolic pathways and novel gene targets for liver fibrosis.

This study shows DPP4 inhibition alters metabolism and inflammation pathways in steatotic hiPSC-derived HLCs, suggesting potential therapeutic benefits for MAFLD.

This study uses transcriptomic profiling to show Resmetirom improves lipid profiles, reduces inflammation and fibrosis, and modulates metabolic and cell death pathways in a MASH mouse model.

This study identifies metabolic biomarkers for CHB-associated MASLD using metabolomics and machine learning, achieving high diagnostic accuracy.

This study shows that rapamycin reduces age-related liver damage caused by a high-fat diet in mice by reversing transcriptional changes and metabolic dysfunction.

This study identifies MAPK15 as a protective factor against MASLD by regulating lipid homeostasis and CD36 expression in the liver.

This study shows liraglutide reduces MASLD symptoms in mice independently of lipophagy, while kombucha also helps but their combination does not provide added benefits.

This study uses a human liver microphysiological system to investigate how insulin, glucose, and free fatty acids contribute to hepatic insulin resistance and its reversibility.

This study shows that loss of AATF reduces MASH in mice by suppressing AKT/mTORC1 signaling and altering lipid metabolism.

This study shows that elevated dietary cholesterol in rats leads to liver lipid crystals, which increase tissue stiffness and fibrosis progression in a model of MASLD.

This study shows that GRK5 inhibition reduces hepatic steatosis in mice on a high-fat diet without affecting body weight or metabolic parameters.

This paper develops an iPSC-based risk predictor for MASLD using lipid accumulation measurements and validates it across three cohorts with varying performance.

This study shows that soluble TREM2 is a biomarker for MASH but not a mediator of its pathogenesis.

Totum-448 reduces hepatic steatosis and inflammation in diet-induced MASLD mice without affecting body weight or microbiota.

This study shows that ablating FGL1 in hepatocytes does not worsen MASLD or HCC, despite increased glucose and metabolic changes in western diet-fed mice.

This study shows thermoneutral housing worsens MASLD in mice by increasing obesity, inflammation, fibrosis, and impairing BAT activation during β3-adrenergic stimulation.

This study shows that ORP2 prevents free cholesterol accumulation in mouse liver, and its absence leads to severe MASH with cholesterol crystals.

This study compares the effects of aerobic exercise and dietary restriction on liver senescence in mice with diet-induced MASLD, finding that dietary restriction is more effective than exercise alone.

This study shows that inhibiting chitinase-1 with OATD-01 reverses metabolic dysregulation and restores homeostasis in MASH animal models.

This study investigates whether ACSL4 deletion in liver cells prevents MASLD progression in mice but finds no significant differences compared to wild-type mice.