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In addition, NSAID-induced enteropathies can involve excessive translocation of luminal contents such as bacteria and their products, bile acids and pepsin, promoting immune activation and ulceration of the intestinal epithelium (Reuter et al

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Non-muscle MLCK isoforms, particularly MLCK1, are highly enriched at the perijunctional actomyosin ring in differentiated villous epithelium and play a dominant role in regulating physiological and pathological barrier dynamics, as selective MLCK1 inhibition or knockdown reduces junctional permeability (Jin and Blikslager, 2020)