| Literature DB >> 31698145 |
Filip Bergqvist1, Ralf Morgenstern2, Per-Johan Jakobsson3.
Abstract
Prostaglandin E2 (PGE2) is a lipid mediator of inflammation and cancer progression. It is mainly formed via metabolism of arachidonic acid by cyclooxygenases (COX) and the terminal enzyme microsomal prostaglandin E synthase-1 (mPGES-1). Widely used non-steroidal anti-inflammatory drugs (NSAIDs) inhibit COX activity, resulting in decreased PGE2 production and symptomatic relief. However, NSAIDs block the production of many other lipid mediators that have important physiological and resolving actions, and these drugs cause gastrointestinal bleeding and/or increase the risk for severe cardiovascular events. Selective inhibition of downstream mPGES-1 for reduction in only PGE2 biosynthesis is suggested as a safer therapeutic strategy. This review covers the recent advances in characterization of new mPGES-1 inhibitors in preclinical models and their future clinical applications.Entities:
Keywords: Cancer; Cyclooxygenase; Inflammation; NSAIDs; Prostaglandin E(2)
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Year: 2019 PMID： 31698145 DOI： 10.1016/j.prostaglandins.2019.106383
Source DB: PubMed Journal: Prostaglandins Other Lipid Mediat ISSN： 1098-8823 Impact factor: 3.072