Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of hepatocytic RKIP depletion on HFD-induced MASLD

ABSTRACT: High-fat diet (HFD) is a risk factor for metabolic dysfunction-associated steatotic liver disease (MASLD), yet the molecular pathways that connect dietary fats to liver dysfunction remain unclear. Hepatocyte-specific RKIP depletion in male mice exacerbates ER stress, resulting in lipid droplets accumulation and MASLD progression.

ORGANISM(S): Mus musculus

PROVIDER: GSE300123 | GEO | 2025/09/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of hepatocytic RKIP depletion on HFD-induced MASLD

Project description:Effect of hepatocytic RKIP depletion on HFD-induced MASLD

| PRJNA1279072 | ENA

RNA-seq data of primary human hepatocytes spheroids from healthy and Metabolic dysfunction associated steatotic liver disease (MASLD) donors following troglitazone treatment

Project description:Primary human hepatocytes from healthy and Metabolic dysfunction associated steatotic liver disease (MASLD) patients (6 donors each) as 3D spheroids treated with troglitazone (3 concentrations, 0.1xCmax, Cmax and 10xCmax) and vehicle for 7 h. Data for Figure 5 in connected publication.

2026-01-16 | E-MTAB-15610 | biostudies-arrayexpress

Transcriptomic profiling of NK cells in CHB and CHB-MASLD

Project description:Clinical evidence suggests that coexistence of metabolic dysfunction-associated steatotic liver disease (MASLD) and chronic hepatitis B (CHB) is associated with more severe liver disease progression, but the underlying immune mechanisms remain incompletely understood. In this study, RNA sequencing was performed on peripheral natural killer (NK) cells isolated from patients with CHB and CHB-MASLD to characterize transcriptomic alterations associated with metabolic dysfunction. Differential expression and pathway analyses were used to identify immune activation programs and candidate signaling pathways linked to NK-cell remodeling in CHB-MASLD.

2026-06-17 | GSE325645 | GEO

Effects of D4-MASLD and D5-MASLD Diets on Rats: Pathway Alterations Similar to Human MASLD

Project description:Animal models are essential to understand the mechanisms underlying the onset and progression of metabolic associated steatotic liver disease (MASLD), a rapidly growing form of chronic liver disease driven largely by the global rise in metabolic syndrome. However, existing animal models for MASLD often fail to accurately reproduce advanced human liver disease, and have varying degrees of clinical relevance. To address this, we have undertaken efforts to create a dietary translational model of MASLD in rats that closely replicates the full MASLD phenotype observed in humans, including advanced fibrosis, portal hypertension, and metabolic syndrome. Three MASLD rat models were developed by sequentially combining a high-fat glucose-fructose diet (HFGFD) with additional factors: lipopolysaccharide, increased cholesterol (Chol), and cholic acid (CA) at different concentrations. Of these, two diets—D4-MASLD (HFGFD + 2% Chol) and D5-MASLD (HFGFD + 2% Chol + 0.1% CA)—effectively replicated MASLD characteristics. Transcriptomic analysis revealed that while both diets significantly altered gene expression compared to controls, D5-MASLD had a greater impact on the activation of inflammation and immune response pathways. The inclusion of CA in D5-MASLD exacerbated pathways related to microbiota changes, intestinal barrier dysfunction, and bacterial translocation. Additionally, comparison of the transcriptomic profiles of these diet-induced rat models with data from MASLD/MASH patients further validated the relevance of these models, establishing a robust platform for studying MASLD pathogenesis and evaluating potential therapeutic interventions.

2026-04-20 | GSE282001 | GEO

Tripartite motif 46 aggravates MASLD progression by suppressing SGPL1- mediated hepatic lipophagy

Project description:Protein post-translational modifications (PTMs) participate in important bioactive regulatory processes and therefore can help elucidate the pathogenesis of Metabolic dysfunction-associated steatotic liver disease (MASLD). Ubiquitination modification plays a vital role in regulating the inflammatory response and fibrosis in MASLD process. Here, we performed multi-omics analysis to demonstated that TRIM46 binds directedly with SGPL1, promoting SGPL1 degradation via K48-linked polyubiquitination which subsequently suppresses the activation of downstream lipophagy signaling cascades in MASLD progression.

2026-05-30 | PXD076863 | Pride

Alternative splicing- and gene fusion-derived neoepitopes in MASLD-associated hepatocellular carcinoma

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD)-driven hepatocellular carcinoma (HCC) exhibits reduced responsiveness to immune checkpoint blockade compared with viral or other etiologies, suggesting underlying differences in tumor immunogenicity and immune evasion. To characterize the immunogenic landscape of MASLD-driven HCC, we profiled transcriptomic data from 120 liver tissue samples, including healthy controls (n = 12), MASLD samples (n = 13), and MASLD-associated HCC samples (n = 95), and investigated the contribution of transcriptome-derived neoantigens to this altered immune landscape, focusing on alternative splicing and gene fusion events as non-canonical sources of tumor-specific epitopes.

2026-06-10 | GSE334651 | GEO

Gene expression profile at single cell level of hepatocytes and non parenchymal cells (NPCs) isolated from a murine model of MASLD

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) embraces different conditions, including metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The landscape of cellular abnormalities occurring in the different stages of MASLD as well as the processes which drive MASLD evolution are not completely clarified. We used single cell RNAsequencing (scRNAseq) to unravel cellular heterogeneity affecting livers during the switching from simple steatosis towads MASH and and MASH-fibrosis.

2025-02-28 | GSE284186 | GEO

Dysregulation of bile acid metabolism exacerbates diet-induced MASLD development in HuR deficient male mouse livers.

Project description:Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a leading cause of hepatocellular carcinoma and liver transplantation worldwide, making identification of intervention strategies and therapeutic treatments essential to reducing morbidity and mortality associated with this disease. RNA binding proteins, like human antigen R (HuR), are ubiquitous and multi-faceted cell-stress regulators. HuR’s role in MASLD development is incompletely understood. This study aims to determine how hepatocyte HuR deficiency drives MASLD progression to Metabolic dysfunction-associated steatohepatitis (MASH). To model MASLD, we fed male hepatocyte-specific HuR knockout mice (HuRHep-/-) and WT control mice with the normal chow diet or the MASLD-inducing high fat, cholesterol, and fructose (HFCF) diet for 16 weeks. The liver transcriptomic profile was mapped using bulk RNA sequencing (RNA seq). After MASLD-inducing diet feeding, bile acid metabolism was modulated, while liver injury and fibrosis markers were increased in male HuRHep-/- mice, relative to WT. Our data suggests that hepatocyte HuR deficiency dysregulates bile acid metabolism and exacerbates MASLD progression.

2026-06-03 | GSE287727 | GEO

Hepatic AKAP1 Deficiency Exacerbates Diet-Induced MASLD by Enhancing GPAT1-mediated Lysophosphatidic Acid Synthesis

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD), closely associated with obesity, can progress to metabolic dysfunction-associated steatohepatitis when the liver undergoes overt inflammatory damage. A-kinase anchoring protein 1 (AKAP1) has been shown to control lipid accumulation in brown adipocytes. However, the role of AKAP1 signaling in hepatic lipid metabolism and MASLD remains poorly understood. Here, we showed that hepatocyte-specific AKAP1 deficiency exacerbated hepatic steatosis and steatohepatitis in male mice subjected to a high-fat diet and fast-food diet, respectively. Mechanistically, AKAP1 directly phosphorylated and inactivated glycerol-3-phosphate acyltransferase 1 (GPAT1) in a PKA-dependent manner, thus suppressing lysophosphatidic acid (LPA) production. Increased endogenous LPA in hepatocytes promoted hepatocellular triglyceride (TG) synthesis and initiated pronounced inflammatory response in Kupffer cells. Restoring hepatic AKAP1 or repressing LPA levels via GPAT1 knockdown alleviated MASLD exacerbation. Overall, AKAP1 plays a protective role against MASLD by inhibiting GPAT1 activity, highlighting the potential of targeting AKAP1/PKA/GPAT1 signalosome for MASLD therapy.

2025-05-26 | PXD062388 | Pride

A Novel Foodstuff Restored Aberrant Dna Methylation Patterns In Western Diet Induced-MASLD Mice

Project description:Background: Aberrant DNA methylation patterns play an important role in the development of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) development. Diets rich in fiber and antioxidants could potentially reverse these patterns. We have previously demonstrated that supplementation with AncestryR, a mixture of Mexican foods (nopal, cocoa, and crickets), exerts a curative effect on MASLD; however, the impact of Ancestry on DNA methylation remains unclear.

2025-12-01 | GSE289914 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data