Liver Disease Diagnosis and Treatment

This study identifies miR-210 as a protective factor against hepatic steatosis by inhibiting CIDEC expression in MASLD.

This study investigates how CDO1-mediated cysteine catabolism in hepatocytes and adipocytes affects diet-induced obesity and fatty liver in mice, finding differential impacts based on tissue-specific manipulation.

This study shows that deleting Pleiotrophin (PTN) protects against high-fat diet-induced liver disease and reveals sex-specific metabolic differences, with females showing greater protection.

The paper develops a deep learning model combining clinical data, gene expression, and DNA methylation to distinguish NASH from steatosis and identifies new genes involved in liver disease severity.

This study shows that TLR4 promotes liver fibrosis in MASLD through mechanisms not involving hepatocytes or inflammatory cells.

This study identifies N-acetyl-phenylalanine (NAPA) as a metabolite that promotes hepatic steatosis in MASLD by disrupting ER-mitochondria calcium coupling and mitochondrial lipid oxidation.

This study shows that liver viscosity decreases before fibrosis in a mouse model of MASH, indicating it as a potential early biomarker.

This study shows that iPSC-derived hepatocytes from MASLD patients show early mitochondrial dysfunction, including reduced oxygen consumption and increased ROS production, independent of PNPLA3 genotype.

This study shows MTARC1 inactivation reduces hepatic triglyceride accumulation and liver injury by promoting lipid droplet degradation through phospholipid remodeling.

This study identifies SAMM50 rs3761472 as a risk factor for MASLD by showing it causes mitochondrial dysfunction and metabolic impairments in mice.

This study shows that c-Fos in hepatocytes promotes MASLD and HCC by altering metabolic pathways and signaling networks in obesity.

This study shows that CLSTN3B promotes lipid droplet maturation in hepatocytes and that its deletion reduces steatohepatitis in mice, with a positive correlation between CLSTN3B expression and MASLD severity in humans.

This study uses single-cell multi-omics to identify cell type-specific regulatory networks and novel therapeutic targets in MASLD.

This study identifies Chi3l1 as a metabolic regulator that differentially affects hepatic macrophage fate in MASLD by modulating glucose metabolism in Kupffer cells.

This study shows ICAM-1 protects against adipose tissue inflammation and insulin resistance but worsens liver inflammation and fibrosis in mice with diet-induced obesity.

This study shows mitochondrial dysfunction causes liver lipid accumulation and inflammation in mtDNA mutator mice without obesity or insulin resistance.

This study shows that PNPLA3-I148M reduces hepatic TAG secretion and protects against cardiac diastolic dysfunction in MASH diet mice, despite promoting liver steatosis.

This study shows that inducing TFEB in Kupffer cells reduces cell death, lipid accumulation, and inflammation in MASLD.

This study investigates the role of CRM1/HMGB1 nuclear translocation in T2D-driven MASLD and shows that inhibiting this pathway reduces HMGB1 release in T2D-NASH.

This study investigates how CIDEB loss-of-function mutations protect against fatty liver disease by enhancing β-oxidation through ATGL and PPARα activation.

This study uses spatial transcriptomics to analyze liver fibrosis stages in MASLD, identifying metabolic reprogramming and senescence signatures linked to fibrosis progression.

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

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.

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

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

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

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.