Liver Disease Diagnosis and Treatment

This study investigates the cellular effects of the PNPLA3-I148M variant, revealing its role in altering lipid droplet-Golgi dynamics and inducing proteomic and transcriptomic changes associated with liver disease.

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 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 study shows that time-restricted feeding reduces NASH symptoms in mice by increasing hepatic IPMK levels and decreasing inflammation.

This study identifies a novel FXR-induced eRNA, FincoR, which mediates the therapeutic effects of hammerhead-type FXR agonists in NASH mice.

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.

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.

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.

This study shows that MCPIP1 protein levels are lower in NAFLD patients' livers compared to controls, but not in PBMCs, and correlate with hepatic steatosis.

This study compares hepatic gene expression in adolescents and adults with NAFLD, finding some similarities but major differences in transcriptomic profiles associated with disease severity.

This study shows that targeting acid ceramidase reduces fibrosis in mouse models of NASH without worsening metabolic features.

This study identifies PKLR as a therapeutic target for NAFLD and validates two drug candidates through in vitro and in vivo experiments.

This study identifies transcription factor networks involved in hepatocyte lipotoxicity using integrative transcriptomic, proteomic, and chromatin accessibility analyses, showing that MAFK and TCF4 deletion protects against fatty acid toxicity.

This study conducts a trans-ancestry GWAS using chronic ALT elevation as a proxy for NAFLD, identifies 77 significant loci, and validates 17 SNPs with histology and imaging data, revealing genetic links to metabolic and inflammatory traits.

This study examines protein expression changes in NASH mice on a high-fat diet with and without mineral supplementation, identifying early molecular alterations and protective effects of minerals.

This study identifies MIR20B as a regulator of PPARA in NAFLD, showing its role in lipid metabolism and potential as a therapeutic target.

The paper uses machine learning to quantify liver fat from MRI data and identifies genetic variants associated with liver fat accumulation and related diseases.

This study shows that deleting Them2 in skeletal muscle reduces weight gain and improves glucose homeostasis on a high-fat diet, but does not prevent hepatic steatosis.

This study investigates the role of Mcpip1 in obesity-induced hepatic steatosis using myeloid and liver-specific conditional knockouts, finding that myeloid depletion leads to systemic inflammation and metabolic dysregulation, while liver-specific depletion has less impact.

The paper identifies AGXT2 as a gene with an anti-fibrotic effect in NAFLD through eQTL screening and functional validation.

This paper performs a meta-analysis of transcriptomic studies to identify sex-based differences in molecular mechanisms during the progression from NAFL to NASH.

The paper develops a mathematical model to show how intra-hepatic functional heterogeneity drives the progression of free fatty acid-induced NAFLD through cascading failure.

The paper investigates the combined effect of three genetic variants on NAFLD progression in patients and in vitro models, finding increased HCC risk and altered lipid and mitochondrial metabolism.