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.

中文翻译：

---

mPGES-1抑制剂综述：从临床前研究到临床应用。

前列腺素E2（PGE2）是炎症和癌症进展的脂质介质。它主要通过环氧合酶（COX）和末端酶微粒体前列腺素E合酶1（mPGES-1）代谢花生四烯酸形成。广泛使用的非甾体抗炎药（NSAIDs）抑制COX活性，导致PGE2生成减少和症状缓解。但是，NSAID会阻断许多其他具有重要生理和解决作用的脂质介体的产生，并且这些药物会引起胃肠道出血和/或增加发生严重心血管事件的风险。选择性抑制下游mPGES-1仅减少PGE2的生物合成被认为是一种更安全的治疗策略。