Published online Feb 14, 2023. doi: 10.3748/wjg.v29.i6.1026
Peer-review started: November 19, 2022
First decision: November 30, 2022
Revised: December 29, 2023
Accepted: January 29, 2023
Article in press: January 29, 2023
Published online: February 14, 2023
Processing time: 82 Days and 14 Hours
One of the significant health issues in the world is the prevalence of ulcerative colitis (UC). UC is a chronic disorder that mainly affects the colon, beginning with the rectum, and can progress from asymptomatic mild inflammation to extensive inflammation of the entire colon. Understanding the underlying molecular mechanisms of UC pathogenesis emphasizes the need for innovative therapeutic approaches based on identifying molecular targets. Interestingly, in response to cellular injury, the NLR family pyrin domain containing 3 (NLRP3) inflammasome is a crucial part of the inflammation and immunological reaction by promoting caspase-1 activation and the release of interleukin-1β. This review discusses the mechanisms of NLRP3 inflammasome activation by various signals and its regulation and impact on UC.
Core Tip: Ulcerative colitis (UC) is a common chronic type of inflammatory bowel disease that affects a significant number of populations. Needing to counteract the UC prevalence, attract scientists to study its pathological mechanism deeply. NLR family pyrin domain containing 3 (NLRP3) inflammasome has been observed to have a crucial role in the pathological features of UC. Targeting NLRP3 inflammasome signals with phytochemicals, plants, probiotics, and chemical agents could be promising candidates for fixing the UC problem.
