Decoding ulcerative colitis pathogenesis through transcriptomics: from dysregulated gene networks to targeted intervention strategies

HCLS1, ITGA4, and PDGFRB may represent core modules involved in T/B cell homing and activation, pro-inflammatory macrophage recruitment, and extracellular matrix responses. These genes interact with upregulated genes to promote the amplification of inflammation, counteracting with downregulated metabolic-related genes. Together, they contribute to the molecular foundation of the inflammatory and metabolic protective phenotype observed in ulcerative colitis.

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Publication Details

Journal
Journal of Translational Autoimmunity
Published
2025-12-08
DOI
https://doi.org/10.1016/j.jtauto.2025.100334
Primary Topic
Inflammatory Bowel Disease
Type
article
Field-Weighted Citation Impact
0.00
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article

Decoding ulcerative colitis pathogenesis through transcriptomics: from dysregulated gene networks to targeted intervention strategies

Yong‐Guang Yang, Yi‐Chun Zhu, Xiang Zhu
Journal of Translational Autoimmunity
Inflammatory Bowel Disease
article

Decoding ulcerative colitis pathogenesis through transcriptomics: from dysregulated gene networks to targeted intervention strategies

Yong‐Guang Yang, Yi‐Chun Zhu, Xiang Zhu
article en

Abstract

HCLS1, ITGA4, and PDGFRB may represent core modules involved in T/B cell homing and activation, pro-inflammatory macrophage recruitment, and extracellular matrix responses. These genes interact with upregulated genes to promote the amplification of inflammation, counteracting with downregulated metabolic-related genes. Together, they contribute to the molecular foundation of the inflammatory and metabolic protective phenotype observed in ulcerative colitis.

Journal of Translational AutoimmunityVol. 12
Zhengzhou University (CN), Fifth Affiliated Hospital of Zhengzhou University (CN)
Openalex Percentile: Top 59%
Inflammatory Bowel Disease
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