Liver Disease Diagnosis and Treatment

The paper uses scRNA-seq to identify zonation changes in fructose metabolism pathways in NAFLD livers, suggesting potential genomic indicators for disease and therapy evaluation.

This study shows Ybx1 promotes adipogenic gene expression in steatotic hepatocytes by interacting with C/EBP and cBAF chromatin-remodeling complexes, contributing to lipid accumulation in liver disease.

This study identifies PD-L1+ neutrophils as mediators of susceptibility to endotoxemia in MAFLD, showing that targeting IFN-γ or PD-L1 reduces inflammation and liver damage.

The paper identifies vitamin B2's role in mitigating AIFM2 deficit-driven hepatocyte death in MASLD using a network modeling approach and validates findings in human cells and clinical data.

The paper shows BRUCE and PTEN together suppress MASLD/MASH by maintaining mitochondrial metabolism and preventing STAT3 activation in HSCs, with DKO mice showing severe liver disease.

This study shows that Top1MT deficiency in mice leads to severe MASH with liver steatosis, inflammation, and fibrosis after a high-fat diet.

This study shows that Mertk deficiency in C-Kit positive hepatic endothelial cells reduces NASH by improving endothelial function and reducing lipid deposition and inflammation.

The paper reanalyzes RNA-seq data from over 800 MASLD livers to identify transcriptomic shifts and risk stratification, revealing molecular switches and immune-related changes associated with disease progression.

This study shows that TCA cycle dysfunction and amino acid catabolism in mice with HFpEF drive hepatic steatosis similar to human NAFLD.

This paper uses AI to develop risk scores for predicting MASLD progression by integrating genetic, anthropometric, and mitochondrial biomarkers.

This study evaluates BI9774, an AMPK activator, in a mouse model of NASH, finding it reduces liver steatosis but not fibrosis and causes cardiac side effects.

This study uses RNA-seq to identify gene expression changes in Efcab4b knockout mice, revealing pathways linked to NAFLD progression and liver injury.

The paper investigates how genetic variants in PNPLA3, MBOAT7, and TM6SF2 affect mitochondrial function in MASLD, showing that restoring these proteins improves mitochondrial bioenergetics and that circulating respirometry reflects hepatic mitochondrial status.

This study examines rare genetic variants in pediatric NAFLD patients with advanced fibrosis but finds no genome-wide significant associations with fibrosis or other histologic features.

This paper develops a 3D multicellular model of NAFLD using hiPSC-derived liver cells to study disease mechanisms and interactions.

This study shows that erythrocyte TLR9 is upregulated in MAFLD and linked to metabolic and inflammatory changes.

This study shows that B cell pyruvate oxidation supports antigen-specific activation, driving inflammation and fibrosis in MASH.

This study evaluates T1 and T2 mapping for assessing liver fibrosis in mice, finding they correlate with fibrosis stages and collagen/protein markers.

This study shows that Rap1a activation prevents fatty liver and NASH by reducing Srebp1 processing and hepatic TG accumulation in obese mice.

The paper integrates single-cell and single-nucleus RNA sequencing data to identify biomarkers associated with NAFLD severity and their intercellular signaling roles.

The paper identifies QSOX1 and IL1RAP as biomarkers for NAFLD severity using gene clustering and validates their plasma ratio as a non-invasive diagnostic tool.

This study identifies EHBP1 as a protective locus against NASH fibrosis by regulating cholesterol metabolism and interacting with other cholesterol-related genes.

This study investigates Lodhrasavam's effects on MASLD using in vitro and in vivo models, showing improvements in lipid metabolism, inflammation, and glucose homeostasis.

This study shows that targeting both DGAT2 in hepatocytes and FASN in stellate cells reduces NASH in mice more effectively than targeting either gene alone.

This study identifies dysfunctional T follicular helper cells in NASH as a driver of intestinal and hepatic inflammation using a mouse model.

This study assesses the effectiveness of PNPLA3 gene therapy in reducing oxidative stress in Huh-7 cells exposed to lipid and alcohol-induced stress.

This study tracks histopathological, biochemical, transcriptomic, and microbiome changes in mice fed a NASH-promoting diet over 30 weeks, revealing progressive NAFLD development and immune/xenobiotic gene expression changes.

This study shows that restoring CYP7B1 expression reduces NASH progression in mice, linking its downregulation to lipid and oxidative stress in the early stages of the disease.

This study identifies BAG6 as a novel target for NASH using in-silico methods, showing its role in reducing fatty acid accumulation and NASH-signature transcripts in Huh-7 cells.

This study shows that excess free fatty acids (FFA) reduce IPMK expression and Akt phosphorylation in mouse hepatocytes, contributing to insulin resistance and NAFLD.