Liver Disease Diagnosis and Treatment

Hepatic HKDC1 Deletion Alleviates Western Diet-Induced MASH in Mice

This study shows that deleting HKDC1 in mice reduces Western diet-induced MASH by improving metabolism and reducing inflammation and fibrosis.

Genomics-Informed Drug Repurposing Strategy Identifies Novel Therapeutic Targets for Metabolic Dysfunction-Associated Steatotic Liver Disease.

The paper identifies 57 druggable targets for MASLD using genetic data and evaluates their therapeutic potential through Mendelian randomization and structural modeling.

KYLO-0603, a novel liver-targeting, thyroid hormone recep-tor-β agonist for the treatment of MASH

Kylo-0603, a THR-β agonist, reduces MASH markers and fibrosis in mice, showing potential as a therapeutic for MASH.

Gcn5l1 governs heart-to-liver crosstalk in cardiometabolic heart failure by modulating cholesterol metabolism

This study identifies Gcn5l1 as a heart-specific factor that modulates cholesterol metabolism and heart-to-liver crosstalk in cardiometabolic heart failure, revealing the heart's role in systemic metabolic dysfunction.

Identification of Growth Differentiation Factor-15 as An Early Predictive Biomarker for Metabolic Dysfunction-Associated Steatohepatitis: A Nested Case-control Study of UK Biobank Proteomic Data

This study identifies GDF15 as an early predictive biomarker for MASH using UK Biobank proteomic data, showing high accuracy up to 10 years before diagnosis.

A Novel Mutation in LXRalpha Uncovers a Role for Cholesterol Sensing in Limiting Metabolic Dysfunction-Associated Steatohepatitis (MASH).

This study shows that a mutation in LXRalpha impairs cholesterol sensing, leading to MASH-like liver disease despite low triglycerides, and that restoring LXR signaling can reverse the condition.

Decoding MASLD Progression: A Molecular Trajectory-Based Framework for Modelling Disease Dynamics

This paper develops a molecular trajectory-based framework to model MASLD progression using transcriptomic and proteomic data, identifying novel biomarkers and mechanistic insights.

LMNA R644C associates with hepatic steatosis in a large cohort and increases cellular lipid droplet accumulation in vitro

Aerobic capacity and exercise mediate protection against hepatic steatosis via enhanced bile acid metabolism.

The paper shows aerobic capacity and exercise enhance bile acid metabolism, which is critical for reducing hepatic steatosis in mice.

PPARalpha-ERRalpha crosstalk mitigates metabolic dysfunction-associated steatotic liver disease progression

This study shows that targeting PPAR and ERR receptors reduces liver fat, fibrosis, and inflammation in MASLD models, suggesting a new therapeutic strategy.

Duodenal organoids from metabolic dysfunction-associated steatohepatitis patients exhibit altered digestive homeostasis

This study examines duodenal organoids from MASH patients and finds altered digestive homeostasis and junctional protein misexpression without barrier dysfunction.

PNPLA3(148M) Promotes Hepatic Steatosis by Interfering with Triglyceride Hydrolysis Through a Gain-of-Function Mechanism

ABHD5 binds PNPLA3 more strongly than ATGL regardless of the I148M variant; steatosis from PNPLA3(148M) needs ATGL and is reversed by ABHD5 overexpression.

NLRP1 is activated by palmitic acid and induced in human metabolic dysfunction-associated steatohepatitis

This study identifies increased NLRP1 expression in MASH liver samples and shows that palmitic acid activates the NLRP1 inflammasome in human cells.

Uttroside B, a US-FDA-Designated Orphan Drug Against Hepatocellular Carcinoma (HCC), Impedes Non-alcoholic Steatohepatitis (NASH) and NASH -Induced HCC

This study demonstrates that Uttroside B alleviates NASH and prevents its progression to HCC in mouse models.

Potential causal links between genetic variants in SAMM50, SUGP1, MAU2, and GATAD2A and liver fat in individuals with normal weight

This study identifies genetic variants associated with liver fat in normal-weight individuals using GWAS and TWAS, highlighting potential causal genes like SAMM50 and novel associations like RFXANK.

Single Cell Transcriptomics Reveal Genomic Indicators of Nonalcoholic Fatty Liver Disease

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.

Ybx1 guides C/EBPα and cBAF chromatin-remodeling complex to promote adipogenic gene expression in steatotic hepatocytes

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.

LncRNA Snhg3 Aggravates Hepatic Steatosis via PPARγ Signaling

This study identifies Snhg3 as a lncRNA that exacerbates hepatic steatosis through PPARγ signaling by modulating SND1 and chromatin remodeling in MASLD.

PDL-1+ Neutrophils mediate susceptibility during endotoxemia in Metabolic Dysfunction Associated Steatotic 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.

A Host Enzyme Reduces Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) by Inactivating Intestinal Lipopolysaccharide

This study shows that AOAH inactivates intestinal LPS, reducing MASLD by preventing hepatic lipid accumulation and altering lipid metabolism gene expression.

Combined stem cell and predictive models reveal flavin cofactors as targets in metabolic liver dysfunction

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

BRUCE liver-deficiency potentiates MASLD/MASH in PTEN liver-deficient background by impairment of mitochondrial metabolism in hepatocytes and activation of STAT3 signaling in hepatic stellate cells

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.

Comparison of Wild-Type and High-risk PNPLA3 variants in a Human Biomimetic Liver Microphysiology System for Metabolic Dysfunction-associated Steatotic Liver Disease Precision Therapy

This study uses a human liver microphysiology system to compare the effects of PNPLA3 variants on MASLD progression and drug response.

Mitochondrial topoisomerase I (Top1MT) prevents the onset of metabolic dysfunction-associated steatohepatitis (MASH) in mice

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

A functional genomic framework to elucidate novel causal non-alcoholic fatty liver disease genes

This study identifies novel causal genes for NAFLD using a combination of GWAS, genetic colocalization, and CRISPRi functional screens.

The ameliorative effect of C-Kit pos hepatic endothelial Mertk deficiency on nonalcoholic steatohepatitis

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.

Hepatic lipopolysaccharide binding protein partially uncouples inflammation from fibrosis in MAFLD

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.

MegaMASLD: An interactive platform for exploring stratified transcriptomic signatures in MASLD progression

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.

Promoting Longevity in Aged Liver through NLRP3 Inflammasome Inhibition Using Tauroursodeoxycholic Acid (TUDCA) and SCD Probiotics

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.

TCA Cycle Dysfunction and Amino Acid Catabolism Drive Hepatic Steatosis in Mice with HFpEF

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