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Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

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Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

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Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
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The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...

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Related Experiment Video

Updated: Jul 4, 2026

Multimodal Quantitative Phase Imaging with Digital Holographic Microscopy Accurately Assesses Intestinal Inflammation and Epithelial Wound Healing
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Unveiling the Cellular and Molecular Insights into Ulcerative Colitis Pathogenesis through Integrative Multi-omics

Yi Han1,2, Junbo Xiao1,2, Jun Yi1,2

  • 1Department of Gastroenterology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.

Combinatorial Chemistry & High Throughput Screening
|July 3, 2026
PubMed
Summary

This study identifies ING4 as a potential causal gene in ulcerative colitis (UC) pathogenesis. Integrating multi-omics data reveals ING4

Keywords:
Single-cell RNA-sequencing dataexpression quantitative trait locimendelian randomizationmulti-omicsprotein quantitative trait lociulcerative colitis

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Published on: February 5, 2021

Area of Science:

  • Genomics and Molecular Biology
  • Immunology and Inflammation
  • Gastroenterology

Background:

  • Single-cell RNA sequencing (scRNA-seq) reveals cellular heterogeneity in ulcerative colitis (UC).
  • Causal relationships between differentially expressed genes (DEGs) and UC pathogenesis require further elucidation.
  • Comprehensive multi-omics integration is needed to understand UC's molecular basis and identify biomarkers.

Purpose of the Study:

  • To explore genomic, transcriptomic, proteomic, and scRNA-seq data for insights into UC molecular mechanisms.
  • To identify potential candidate biomarkers for UC.
  • To investigate the causal relationship between DEGs and UC pathogenesis using Mendelian randomization.

Main Methods:

  • Analysis of the GSE125527 scRNA-seq dataset for cell identification and DEG analysis.
  • Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data (ieu-a-32) with expression and protein quantitative trait loci (eQTL/pQTL) data.
  • Integration of multi-omics data and in vitro/in vivo validation of candidate genes.

Main Results:

  • Identification of 1,905 DEGs across 5 cell subtypes from 48,576 cells.
  • FCN1 and ING4 identified as causally associated with UC through MR and eQTL/pQTL analysis.
  • ING4 demonstrated reduced expression in UC tissues and LPS-treated cells, impacting NF-κB pathway and iNOS release, suggesting a role in inflammation.

Conclusions:

  • ING4 is a candidate gene with a genetically supported link to UC, connecting immune variation to epithelial inflammation.
  • ING4 serves as a promising candidate biomarker and potential therapeutic target for UC.
  • Multi-omics data integration is crucial for understanding UC pathogenesis.