Targeting the NLRP3 inflammasome as new therapeutic avenue for inflammatory bowel disease - 16/04/21
, Ying Wang b, c, ⁎, 3 Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
The incidence and prevalence of inflammatory bowel disease (IBD) are increasing worldwide. Current approved medication for IBD treatment in the clinic mainly includes corticosteroids and neutralization antibodies to pro-inflammatory cytokines. However, drug resistance and severe side effect hinder long-term efficacy of these agents. The NOD-like receptor family pyrin domain containing protein 3 (NLRP3) is exclusively expressed in several inflammatory and autoimmune diseases. Excessive expression, aberrant activation, polymorphism, and gain-of-function mutation of the NLRP3 inflammasome contribute to IBD pathogenesis. In this article, we summarize the regulatory factors to NLRP3, and review recently developed NLRP3 inhibitors and their preclinical and clinical applications in treating inflammatory and autoimmune diseases. We present our views on the therapeutic potential of NLRP3 inhibitors as emerging therapeutic avenue for IBD.
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Highlights |
• | NLRP3 inflammasome activation contributes to the pathogenesis of IBD. |
• | Multiple factors regulate activation and expression of NLRP3 at transcription, translation, and post-translation levels. |
• | Small molecule inhibitors of NLRP3 are tested in preclinical and clinical IBD models. |
• | Targeting NLRP3 inflammasome is of great potential for the management of IBD. |
Abbreviation : AD, ASC, BRET, BMDM, BTK, CD, CAPS, cAMP, DUB, DSS, DNBS, FDA, GSDMD, IBD, IFLX, IL, LRR, LPS, miRNA, mtDNA, MSU, NEK7, NLR, OA, ROS, RA, STING, NLRP3, TNF, TXNIP, USP, UC, 3′UTR, WT
Keywords : NLRP3, Inflammatory bowel disease, Small molecule inhibitor, Targeted therapy
Plan
Vol 138
Article 111442- juin 2021 Retour au numéro
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