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COX-2–PGE2 Signaling Impairs Intestinal Epithelial Regeneration and Associates with TNF Inhibitor Responsiveness in Ulcerative Colitis
Author(s) -
Yuan Li,
Christoffer Soendergaard,
Fredrik Bergenheim,
David M. Aronoff,
Ginger L. Milne,
Lene Riis,
Jakob Benedict Seidelin,
Kim B. Jensen,
Ole Haagen Nielsen
Publication year - 2018
Publication title -
ebiomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.596
H-Index - 63
ISSN - 2352-3964
DOI - 10.1016/j.ebiom.2018.08.040
Subject(s) - tumor necrosis factor alpha , cancer research , medicine , immunology , cyclooxygenase , signal transduction , inflammatory bowel disease , proinflammatory cytokine , biology , inflammation , microbiology and biotechnology , disease , enzyme , biochemistry
Inhibition of tumor necrosis factor-α (TNF) signaling is beneficial in the management of ulcerative colitis (UC), but up to one-third of patients do not have a clinical response of relevance to TNF inhibitors during induction therapy (i.e. primary non-responders [PNRs]). Through production of prostaglandins (PGs) and thromboxanes, cyclooxygenase-2 (COX-2) affects inflammation and epithelial regeneration and may in this way be implicated in treatment resistance to TNF inhibitors.

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