Journal
PROSTAGLANDINS & OTHER LIPID MEDIATORS
Volume 147, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2019.106383
Keywords
Prostaglandin E-2; NSAIDs; Cyclooxygenase; Cancer; Inflammation
Categories
Funding
- Swedish Research Council [2015-03955, 2017-01391, 2017-02577]
- Innovative Medicines Initiative (EU/EFPIA, ULTRA-DD) [115766]
- Stockholm County Council (ALF) [20160378]
- Swedish Rheumatism Association [R-755861]
- King Gustaf V's 80 Years Foundation
- Swedish Cancer Society [CAN2016/739]
- Karolinska Institutet
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Prostaglandin E-2 (PGE(2)) 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 PGE(2) 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 PGE(2) 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.
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