Liver Disease Diagnosis and Treatment

This study creates a human iPSC-derived hepatocyte model with the TM6SF2 E167K mutation to study its effects on lipid metabolism and MASLD.

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.

This study shows that reducing hepatic LBP in mice limits inflammation but not fibrosis in MAFLD, suggesting inflammation may not be a primary driver of fibrosis.

This study identifies antigen-driven CD8+ T cell clonal expansion in human and mouse MASH, showing their activation and functional differentiation in liver disease.

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 examines the effects of SCD Probiotics and TUDCA on aged rat liver tissue, showing reduced inflammasome activity and improved biomolecular profiles through histological and molecular analyses.

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 shows that activating estrogen receptors in male mice reduces HFD-induced liver steatosis by modulating gene expression and TEAD1, suggesting TEAD1 inhibition as a therapeutic strategy for NAFLD.

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 study investigates MLKL's non-necroptotic roles in diet-induced obesity and liver disease using a HFHFrHC mouse model, finding dose-dependent effects on inflammation and metabolic parameters.

This paper shows that miR-26b deficiency worsens MASH in mice, and that miR-26b mimic-loaded LNPs can reverse these effects.

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 uses multi-omics approaches to analyze how dietary restriction and sleeve gastrectomy affect the cellular and metabolic changes in steatotic livers in rats and humans.

This study identifies LysTTT-5tRF and miR-194-5p as co-regulators of hepatic steatosis through beta-Klotho and Perilipin 2, showing their cooperative roles in lipid metabolism.

The paper evaluates three NAFLD liver organoid models using single-cell transcriptomics, finding TGF-β1 induces fibrosis while OA reduces fibrotic signatures.

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

The paper identifies betacellulin as a target of omega-3 fatty acids in reducing NASH by suppressing inflammation and fibrosis through mechanisms involving hepatic stellate cells and macrophages.

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

This study creates a LEPTIN-deficient pig model of NAFLD and shows that AMPK signaling plays a key role in hepatic fibrosis progression.

This study uses zebrafish models to investigate the role of lipid genes in fatty liver disease, finding that gene knockdowns enhance ethanol and high fat diet-induced liver damage.

This study shows that MCT1 in hepatic stellate cells promotes collagen expression in NASH, while hepatocyte MCT1 does not significantly affect fibrosis.

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.