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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

ABSTRACT: IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

PROVIDER: PRJNA1015543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26037700_1.fastq.gz	Fastqsanger.gz
	SRR26037700_2.fastq.gz	Fastqsanger.gz
	SRR26037701_1.fastq.gz	Fastqsanger.gz
	SRR26037701_2.fastq.gz	Fastqsanger.gz
	SRR26037694_1.fastq.gz	Fastqsanger.gz

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

| PRJNA1015522 | ENA

IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

| PRJNA1015547 | ENA

IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-01 | GSE242930 | GEO

IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

Project description:We found IL22 could reduce intestinal fatty acid transporters expression. We used single cell RNA sequencing (scRNA-seq) to analyze the cell population and gene expression with Fc or IL-22Fc treatment.

2024-08-01 | GSE242927 | GEO

IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

Project description:IL22 induces antimicrobial peptides which influnce microbiota. We used 16s rRNA gene sequencing (16s DNA-seq) to analyze the microbiota with Fc or IL-22Fc treatment.

2024-08-01 | GSE242929 | 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

Intestinal organoid expression data from patients with MASLD-cirrhosis versus non-fibrotic MASLD

Project description:This study aimed to establish and characterize an in vitro model of human intestinal organoids isolated from duodenal samples of patients with non-fibrotic MASLD and those with MASLD-cirrhosis. Whole transcriptome analysis and the energetic and redox status of the organoids were assessed to characterize intestinal functional impairment in the context of MASLD. We used microarrays to detail the whole transcriptome dysregulation underlying intestinal dysfunction in organoids isolated from chirrotic versus non-fibrotic MASLD patients.

2025-09-04 | GSE299719 | GEO

Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in mice

Project description:Accumulating evidence suggests that a compromised intestinal epithelial barrier (IEB) contributes to the progression of metabolic dysfunction-associated steatotic liver disease (MASLD); however, the exact mechanisms remain unclear. Here we reveal that intestinal mucin 1 (MUC1) levels and glycosylation are decreased in both humans and mice with MASLD. Enterocyte-specific Muc1 knockout aggravates high-fat diet (HFD)-induced IEB impairment and MASLD progression in mice. Mechanistically, HFD feeding reduces the glycosylation of intestinal epithelial MUC1, triggering its clathrin-mediated endocytosis and NEDD4-mediated lysosomal degradation, which subsequently induces β-Catenin degradation and ultimately impaires the IEB. Notably, enterocyte-specific overexpression of cytoplasmic-tail-deleted MUC1 protects against IEB impairment and mitigates MASLD progression. These findings indicate that reduced intestinal epithelial MUC1 levels facilitate the progression of MASLD. Preserving the glycosylation and levels of intestinal MUC1 to maintain IEB integrity is a potential therapeutic strategy to explore for MASLD.

2025-12-14 | PXD066810 | Pride

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

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

| PRJNA1186599 | ENA

A Microphysiological Model of Human MASLD Reveals Paradoxical Response to Resmetirom

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic disease with multiple etiologies, stemming from the interplay between local and systemic genetic, diet, and gene-environment interactions. To understand the progression of MASLD in a controlled setting, we utilized a human liver microphysiological system (MPS) to establish a physiologically relevant metabolic baseline and probe how primary human hepatocytes respond to perturbations in insulin, glucose, and free fatty acids (FFAs). Replicate liver MPS were maintained in media with either 200 pM or 800 pM insulin for up to 3 weeks alone and in combination with standard glucose (5.5 mM), hyperglycemia (11 mM glucose), normal (20µM) and elevated FFA (100 µM). Together, hyperinsulinemia along with elevated glucose and FFAs, induces the release of pro-inflammatory chemokines, accumulation of triglycerides, and predisposes hepatocytes to insulin resistance. Treatment with the thyroid receptor ß agonist resmetirom normalizes hepatic fat content and partially rescues insulin sensitivity, but paradoxically induces higher CXCL1 and IL8 expression in male and female donors. In aggregate, our enhanced in vitro MPS model establishes a metabolic baseline and perturbed condition that recapitulates a spectrum of phenotypes observed in MASLD, offering improved quantification and insight into disease progression with relevance to human physiology.

2025-12-15 | GSE313774 | GEO

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