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Review demonstrates that adherens junction breakdown drives intestinal inflammation, indicating that epithelial barrier defects trigger intrinsic inflammatory bowel disease pathways.
Adherens junctions (AJs) play a fundamental role in epithelial physiology, supporting cell-cell cohesion and communication. There has been a long-standing concept that loss of functioning AJs may contribute to epithelial inflammation. In the context of the intestine, experimental disruption of the E-cadherin adhesion system induces inflammation, while E-cadherin and its regulators have been identified as susceptibility genes for inflammatory bowel disease. In this article, we briefly consider how AJ dysfunction may serve as a driver in the pathogenesis of IBD, especially in light of emerging evidence that AJs can regulate intrinsic inflammatory programs in the intestinal epithelium.
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Haslam et al. (2026) studied this question.
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