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Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease

ABSTRACT: Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease

PROVIDER: PRJNA1209064 | ENA |

REPOSITORIES: ENA

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Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease

Project description:DNA demethylation is regulated by the TET family proteins, whose enzymatic activity requires 2-oxoglutarate (2-OG) and iron that both are elevated in MASLD. We aimed to investigate liver TET1 in MASLD progression. Depleting TET1 substantially alleviated MASLD progression. Whole body Knockout of TET1 (TKO) slightly improved diet induced obesity and glucose homeostasis. Intriguingly, hepatic cholesterols, triglycerides, were significantly decreased upon TET1 depletion. Moreover, targeting TET1 with a small molecule inhibitor significantly suppressed MASLD progression. Liver TET1 plays a deleterious role in MASLD, suggesting the potential of targeting TET1 in hepatocytes to suppress MASLD.

2025-03-04 | GSE286394 | GEO

Oxidised apolipoprotein peptidome characterise metabolic dysfunction-associated steatotic liver disease.Oxidised apolipoprotein peptidome characterise metabolic dysfunction-associated steatotic liver disease.

Project description:A proteomic and peptidomics analysis of serum from patients suffering from metabolic dysfunction-associated steatotic liver disease. Proteomics was performed initially on a set of patients with varying degrees of liver disease. Following close analysis of the results, a peptidomics based analysis was performed and identified significant numbers of degraded and oxidised peptides from apolipoproteins. A more targeted peptidomics analysis was performed on a larger cohort and the oxidation status of small apolipoproteins demonstrated a high accuracy of precision for liver disease diagnosis.

2025-01-21 | PXD052061 | Pride

Deep proteome profiling of metabolic dysfunction-associated steatotic liver disease

Project description:Analyze human biopsies for the investigation of metabolic dysfunction-associated steatotic liver disease (MASLD). We also analyzed plasma samples for biomarker discovery. And analyzed the role of the impact of the adipose tissue on plasma proteins in relation to MASLD

2025-03-05 | PXD051911 | Pride

Transcriptional profiling of liver obtained from a mouse model for metabolic dysfunction-associated steatotic liver disease

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent hepatic disorder worldwide and closely associated with type 2 diabetes mellitus (T2DM). The pathogenesis of MASLD is multifaceted and its treatment options are very limited. Consequently, it is urgent to identify novel therapeutic targets and develop effective treatment strategies. RNA sequencing analysis was performed to understand the transcriptomic changes in a mouse model of MASLD.

2025-01-20 | GSE279512 | GEO

Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

Project description:Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

| PRJNA1094958 | ENA

Targeting Senescent Hepatocytes for Treatment of Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-organ Dysfunction

Project description:Senescent hepatocytes accumulate in metabolic dysfunction-associated steatotic liver disease (MASLD) and are linked to worse clinical outcomes. However, their heterogeneity and lack of specific markers have made them difficult to target therapeutically. Here, we define a senescent hepatocyte gene signature (SHGS) using in vitro and in vivo models and show that it tracks with MASLD progression/regression across mouse models and large human cohorts. Single-nucleus RNA-sequencing and functional studies reveal that SHGS+ hepatocytes originate from p21+ cells, lose key liver functions and release factors that drive disease progression. One such factor, GDF15, increases in circulation alongside SHGS+ burden and disease progression. Through chemical screening, we identify senolytics that selectively eliminate SHGS+ hepatocytes and improve MASLD in mice. Notably, SHGS enrichment also correlates with dysfunction in other organs. These findings establish SHGS+ hepatocytes as key drivers of MASLD and highlight a potential therapeutic strategy for targeting senescent cells in liver disease and beyond.

2025-02-21 | GSE288534 | GEO

Metabolic dysfunction-associated steatotic liver disease may increase intrahepatic interferon gene signatures in patients with chronic hepatitis B

Project description:As metabolic dysfunction-associated steatotic liver disease (MASLD) frequently co_x0002_occurs in patients with chronic hepatitis B (CHB), the interplay between these two common liver conditions remains largely unexplored. A recent study suggest that MASH comorbidity can reduce intrahepatic interferon pathway activity and macrophage gene signatures in HBeAg_x0002_negative chronic HBV (ENEG) patients, potentially contributing to persistent infection and fibrosis. However, it remains unclear whether this phenomenon also occurs in MASLD with CHB patients.

2025-01-27 | GSE288077 | GEO

Aging Promotes Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-Organ Dysfunction by Inducing Ferroptotic Stress

Project description:Aging Promotes Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-Organ Dysfunction by Inducing Ferroptotic Stress

| PRJNA1091908 | ENA

Targeting Senescent Hepatocytes for Treatment of Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-organ Dysfunction

Project description:Targeting Senescent Hepatocytes for Treatment of Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-organ Dysfunction

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A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [RNA-seq]

Project description:The lack of an appropriate preclinical model of metabolic dysfunction-associated steatotic liver disease (MASLD) that recapitulates the whole disease spectrum impedes exploration of disease pathophysiology and the development of effective treatment strategies. Considering the fact that MASLD patients accompanying type 2 diabetes mellitus (T2DM) have high risk of developing metabolic dysfunction-associated steatohepatitis (MASH), advanced fibrosis, and HCC, we treated low-dose streptozotocin (STZ; 40 mg/kg) for 5 consecutive days and subsequently fed a high-fat diet (HFD) to male C57BL/6J mice at 7 weeks of age (STZ+HFD). STZ+HFD mice gradually developed fatty liver, MASH, hepatic fibrosis, and hepatocellular carcinoma (HCC) in the context of metabolic dysfunction. In particular, from 20 weeks of age, MASH was evident, and from 32 weeks of age, advanced fibrosis was developed. At 38 weeks, a proportion of STZ+HFD mice developed HCC, which was subsequently observed in all mice up to 68 weeks of age. Furthermore, the hepatic transcriptomic features of STZ+HFD mice closely reflected those of obese patients with T2DM, MASH and MASLD-related HCC. Notably, dietary changes and tirzepatide administration alleviated MASH, hepatic fibrosis, and hepatic tumorigenesis in STZ+HFD mice. In conclusion, a murine model recapitulating the main histopathologic, transcriptomic, and metabolic alterations observed in MASLD patients with metabolic dysfunction was successfully established.

2024-06-17 | GSE246221 | GEO

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