Liver Disease Diagnosis and Treatment

Sex- and hepatocyte PPARγ-dependent effects of an obesogenic dietary approach to induce MASH with fibrosis in mice

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

Integrative multi-omics and multi-trait analysis prioritizes regulatory mechanisms and genes for metabolic dysfunction-associated steatotic liver disease

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.

Prime Editing Models the MTARC1 A165T Variant in Human Liver Organoids, Demonstrating Reduced Steatosis, Inflammation, and Fibrosis

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

Targeting Microbial Bile Salt Hydrolase Reprograms Bile Acid Metabolism and Ameliorates Metabolic Dysfunction-Associated Steatohepatitis in Mice

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.

Physiologically relevant media are associated with overlapping metabolic responses in primary human hepatocytes and Huh7 cells

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.

Myeloid HDAC7 drives liver inflammation and systemic glucose dysregulation during diet-induced obesity

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

Metabolomic, Lipidomic, and Enterohormone Changes in the Progression from MASLD to MASH

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.

Hyperactivated Glycolysis Drives Spatially-Patterned Kupffer Cell Depletion in MASLD

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

Recapitulation of clinical and molecular hallmarks of lipid-induced hepatic insulin resistance in a zonated, vascularized human liver acinus microphysiological system during metabolic dysfunction-associated steatotic liver disease (MASLD) progression

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

CD4+ T cells promote fibrosis during metabolic dysfunction-associated steatohepatitis

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.

Global molecular landscape of early MASLD progression in obesity

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.

DPP4 inhibition affects metabolism and inflammation associated pathways in hiPSC-derived steatotic HLCs

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

Modulation of metabolic, inflammatory, fibrotic and cell death pathways by Resmetirom in metabolic dysfunction-associated steatohepatitis (MASH): A transcriptomic profiling study

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.

Metabolomics-Guided Machine Learning Reveals Diagnostic and Mechanistic Biomarkers in CHB with MASLD

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

Rapamycin Reverses the Hepatic Response to Diet-Induced Metabolic Stress That Is Amplified by Aging.

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.

MAPK15 Protects Against The Development Of Metabolic Dysfunction-Associated Steatotic Liver Disease

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

Liraglutide exerts protective effects on MASLD independently of lipophagy, and the combination with kombucha presents no additional advantage

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

A Microphysiological Model of Progressive Human Hepatic Insulin Resistance

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.

Hepatic loss of AATF attenuates MASH by suppressing AKT/mTORC1 signaling and reprogramming lipid metabolism

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

Intrahepatic crystals from elevated dietary cholesterol are sufficient to stiffen the liver

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.

Pharmacological inhibition of G protein-coupled receptor kinase 5 decreases high-fat diet-induced hepatic steatosis in mice

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

Predicting Metabolic Dysfunction Associated Steatotic Liver Disease Risk Using Patient-Derived Induced Pluripotent Stem Cells

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

Soluble TREM2 is a biomarker but not a mediator of fibrosing steatohepatitis

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

Totum-448, a polyphenol-rich plant extract, decreases hepatic steatosis and inflammation in diet-induced MASLD mice

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

Ablation of hepatocyte derived-FGL1 does not aggravate metabolic dysfunction-associated steatotic liver disease and hepatocellular carcinoma

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.

Effect of thermoneutral housing on MASLD severity, hepatic gene expression, and BAT activation during β3-adrenergic stimulation in mice

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

ORP2 regulates free cholesterol accumulation in hepatocytes during MASH

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

Exercise alleviates liver senescence but does not outmatch the effect of dietary restriction in diet-induced MASLD

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.

Chitinase-1 inhibition reverses metabolic dysregulation and restores homeostasis in MASH animal models

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

The ferroptosis mediator ACSL4 fails to prevent disease progression in mouse models of MASLD

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