Ulcerative colitis(UC)is a chronic inflammatory bowel disease characterized by non-spe-cific,persistent inflammation in the intestines.This chronic inflammation often increases the risk of serious com-plications such as colorectal cancer.Dysplasia acts as a driver of cancer development and plays a connecting role in the occurrence and development of chronic intestinal inflammation and colorectal cancer.Cell proliferation/ap-optosis imbalance is the driving factor for dysplasia development.The abnormal proliferation/apoptosis of intestinal mucosal epithelial cells may be affected by cyclooxygenase-2(COX-2),tumor suppressor gene p53,or both.Therefore,reasonable regulation of COX-2/p53 axis may be a key to achieving intestinal mucosal prolifera-tion/apoptosis balance.This article discusses the effects and mechanism of COX-2 and p53 in regulating the oc-currence and development of dysplasia in UC from the proliferation/apoptosis imbalance of intestinal mucosal epi-thelial cells,aiming to provide a reference for understanding the mechanism of dysplasia in UC and developing targeted therapeutic drugs.
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