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Testing the contribution of FGL1 to the pathogenesis of metabolic dysfunction-associated steatotic liver disease and hepatocellular carcinoma

ABSTRACT: Testing the contribution of FGL1 to the pathogenesis of metabolic dysfunction-associated steatotic liver disease and hepatocellular carcinoma

PROVIDER: PRJNA1232123 | ENA |

REPOSITORIES: ENA

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Testing the contribution of FGL1 to the pathogenesis of metabolic dysfunction-associated steatotic liver disease and hepatocellular carcinoma

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) begins with simple steatosis, which can progress to hepatocellular carcinoma (HCC). The pathogenesis of MASLD alters the secretion of hepatokines such as fibrinogen-like 1 (FGL1), a candidate mediator of liver steatosis and hyperglycemia. To investigate the contribution of FGL1 to liver diseases, we compared wild-type mice to mice with hepatocyte-specific deletion of Fgl1 subjected to a steatosis or HCC experimental protocol. We found that mice deficient for Fgl1 in hepatocytes showed higher levels of plasma glucose, pronounced metabolic alterations and liver injury when fed a western diet compared to their wild-type counterparts. However, both genotypes exhibited a similar lipid deposition in the liver. Similarly, wild type and Fgl1-deficient mice displayed comparable liver alterations during HCC progression. We observed that FGL1 expression was repressed during MASLD progression in mice and human concomitantly with the severity of liver injury. Altogether, these findings suggest that FGL1 is not a major contributor to the pathogenesis of MASLD and HCC.

2025-08-27 | GSE291163 | GEO

Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1

Project description:The molecular mechanisms underlying the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) remain largely unclear. Emerging evidence suggests that microRNAs (miRNAs) play a critical role in transcriptional regulation by targeting genes involved in MASLD and other metabolic disorders, this study aims to elucidate the role of miR-93 in lipid metabolism and its impact on MASLD progression.

2025-04-14 | GSE277560 | GEO

Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1

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Kisspeptin Mitigates Hepatic De Novo Lipogenesis in Metabolic Dysfunction Associated Steatotic Liver Disease

Project description:Emerging evidence suggests that the peptide hormone kisspeptin, signaling via the kisspeptin 1 receptor (KISS1R), decreases hepatic steatosis and protects against metabolic dysfunction-associated steatotic liver disease (MASLD). De novo lipogenesis (DNL) is a key contributor to the pathogenesis of MASLD. This study aimed to determine whether kisspeptin treatment of obese, diabetic mice directly attenuates DNL. DNL was assessed in kisspeptin-treated (KPA) or phosphate-buffer saline (PBS)-treated mouse livers, using a mouse model of MASLD employing metabolic tracing using 2H2O-enriched water and mass spectrometry. Kisspeptin-treated steatotic livers demonstrated a decrease in DNL of free fatty acids (FFA), known to be associated with type 2 diabetes, steatosis, and hepatocellular carcinoma. Enhancement of KISS1R signaling has a therapeutic effect in limiting DNL, suggesting a crucial role in restricting the pathogenesis and progression of MASLD.

2025-05-29 | MSV000098033 | MassIVE

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

Dysregulation of GTPase-activating protein-binding protein1 in the pathogenesis of metabolic dysfunction-associated steatotic liver disease

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

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Deep proteome profiling of metabolic dysfunction-associated steatotic liver disease

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Dysregulation of GTPase-activating protein-binding protein1 in the pathogenesis of metabolic dysfunction-associated steatotic liver disease

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are two common liver disorders characterized by abnormal lipid accumulation. Our study found reduced levels of GTPase-activating protein-binding protein1（G3BP1）in patients with MASLD and MASH, suggesting its involvement in these liver disorders. Hepatocyte-specific G3BP1 knockout (G3BP1 HKO) mice had more severe MASLD and MASH than their corresponding controls. Intriguingly, the G3BP1 HKO MASLD model mice exhibit dysregulated autophagy, and biochemical analyses demonstrated that G3BP1 promotes autophagosome-lysosome fusion through direct interactions with the SNARE proteins STX17 and VAMP8. We also show that hepatic knockout of G3BP1 promotes de novo lipogenesis, and ultimately found that G3BP1 is required for the nuclear translocation of the well-known liver-lipid-regulating transcription factor TFE3. Taken together, our results suggest that G3BP1 should be investigated as a potential target for developing medical interventions to treat MASLD and MASH.

2025-08-06 | GSE304454 | GEO

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