ArticleCells2025
In Vitro Inhibition of Endoplasmic Reticulum Stress: A Promising Therapeutic Strategy for Patients with Crohn's Disease.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Necroptosis-related diseases are regulated by the unfolded protein response during endoplasmic reticulum stress.Genes & diseases · 2027Review
- Biogenesis of TNF-α-insights into proteostasis and inflammation.The FEBS journal · 2026Review
- Role and progression of bile acid metabolism in mediating Th17/Treg homeostasis in inflammatory bowel disease.iScience · 2026Review
- Endoplasmic reticulum stress and exosomes secretion in the pathogenesis of inflammatory bowel disease: a concise summary of research findings.Frontiers in pharmacology · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundCrohn's disease (CD) is an inflammatory bowel disease marked by an abnormal immune response and excessive pro-inflammatory cytokines, leading to impaired protein processing and endoplasmic reticulum (ER) stress. This stress, caused by the accumulation of misfolded proteins, triggers the unfolded protein response (UPR) through IRE1/Xbp-1, PERK/eIF2α, and ATF6 pathways, which are linked to intestinal inflammation. This study aimed to investigate ER stress in CD patients' intestinal mucosa and evaluate phenylbutyrate (PBA) as an ER stress inhibitor.
methodsColon biopsies from CD patients and controls were cultured under five conditions, including 4-PBA treatments. Real-time PCR, cytokine level, and immunohistochemistry were performed.
resultsImmunohistochemistry revealed that ER stress was activated in CD patients' intestinal epithelial cells and lamina propria cells. PERK/eIF2α, but not IRE1/Xbp-1 or ATF6, was upregulated in CD patients compared to controls. UPR-related genes (STC2, CALR, HSPA5, HSP90B1) were also elevated in CD patients. PBA treatment significantly reduced ER stress and UPR markers while decreasing apoptotic markers like DDIT3. Pro-inflammatory cytokines, such as IL-1β, IL-6, IL-17, TNF- α, and sCD40L, were significantly reduced after PBA treatment.
conclusionER stress and UPR pathways are activated in CD colonic mucosa, and PBA reduces these markers, suggesting potential therapeutic benefits for CD-related inflammation.
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