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 combines stem cell models and computational predictions to identify flavin cofactors as therapeutic targets for metabolic liver dysfunction.

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 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 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.

This study identifies BATF's role in alleviating hepatic steatosis by inhibiting PD1 and promoting energy metabolism in NAFLD.

This study uses Mendelian randomisation to investigate the causal relationship between circulating amino acid levels and non-alcoholic fatty liver disease risk, finding higher alanine and lower glutamine levels are associated with increased and decreased risk, respectively.

This study shows that early exercise training in mice worsens hepatic inflammation in early NAFLD, while late training does not, suggesting timing affects exercise benefits.

This study shows that recombinant Orm2 treatment reduces hepatic steatosis, inflammation, and fibrosis in NASH models by inhibiting the Erk1/2-PPARγ-Cd36 pathway.

This study uses single-nucleus ATAC-seq and machine learning to identify gene regulation modules and core genes in NAFLD progression in rats.

The paper uses a multi-omics approach to analyze proteomic, phosphoproteomic, and lipidomic data from mouse livers to identify dysregulated protein phosphorylation and lipid metabolism in diet-induced obesity.