Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha 410011, P.R. China.
Curr Vasc Pharmacol. 2013 Jan;11(1):105-11.
Epoxyeicosatrienoic acids (EETs) have been shown to play a role in cardiovascular protection by reducing ischemia reperfusion injury, producing anti-inflammatory effects, and promoting angiogenesis. EETs are regulated through conversion to less active corresponding diols by soluble epoxide hydrolase (sEH). Inhibition of sEH enhances the beneficial properties of EETs and has been investigated as a possible treatment for cardiovascular diseases.
sEH inhibitors (sEHIs) have anti-inflammatory effects by stabilizing anti-inflammatory EETs. Additionally, sEHIs strongly inhibit and reverse cardiac hypertrophy. sEHIs have been shown to protect myocardial cells from ischemiareperfusion injury, treat atherosclerosis and prevent the development of hypertension. sEHIs promote blood vessels to release bradykinin via an EET-mediated STAT3 signaling pathway to elicit tolerance to ischemia.
Inhibition of sEH has been shown to improve several aspects of cardiovascular diseases, including inflammation, hypertension, cardiac hypertrophy and atherosclerosis. For this reason, sEHIs are promising new pharmaceutical for the treatment of cardiovascular diseases.
环氧二十碳三烯酸(EETs)通过减少缺血再灌注损伤、产生抗炎作用和促进血管生成,在心血管保护中发挥作用。EETs 通过可溶性环氧化物水解酶(sEH)转化为活性较低的相应二醇而受到调节。抑制 sEH 可增强 EETs 的有益特性,并已被研究作为心血管疾病的一种可能治疗方法。
sEH 抑制剂(sEHIs)通过稳定抗炎性 EETs 发挥抗炎作用。此外,sEHIs 强烈抑制和逆转心肌肥厚。sEHIs 已被证明可保护心肌细胞免受缺血再灌注损伤,治疗动脉粥样硬化并预防高血压的发展。sEHIs 通过 EET 介导的 STAT3 信号通路促进血管释放缓激肽,从而产生对缺血的耐受性。
抑制 sEH 已被证明可改善心血管疾病的多个方面,包括炎症、高血压、心肌肥厚和动脉粥样硬化。因此,sEHIs 是治疗心血管疾病有前途的新型药物。