XG, SimMK.Des-aspartate-angiotensin I causes specific release of PGE2 and PGI2 in HUVEC via the angiotensin AT1 receptor and biased agonism.Eur
- Wen Q, Lee KO, SimSZ, Xu
- J Pharmacol
Prostacyclin is a strong cardioprotective hormone released by the endothelium of the blood vessels. Prostacyclin is present in equilibrium with several vasoactive agents in cardiovascular system. In recent years, prostacyclin (PGI2) has also been shown to enhance differentiation and inhibit proliferation in vascular smooth muscle cells. In addition to these well-described homeostatic roles within the cardiovascular system, prostacyclin (PGI2) also plays an important role as an inflammatory mediator. In this review, the focus on the contribution of prostacyclin (PGI2) as both a patho-physiological mediator in three major inflammatorymediated disease processes, namely rheumatoid arthritis, where it promotes disease progression , along with pulmonary vascular disease and atherosclerosis, where it inhibits disease progression. On the other hand, CDP-DAG synthases (CDS) are enzymes that catalyze the conversion of phosphatidic acid (PA) to CDPdiacylglycerol (CDP-DAG). Both PA and CDP-DAG serve critical roles in cellular functions.This article reviews the possibility of interaction with CDP diacylglycerol and it appears that de novo synthesis of PGI2 or its congeners occurs in specialized cells under patho-physiological conditions.