雌激素
内分泌学
内科学
雌激素受体
受体
细胞生物学
G蛋白偶联受体
医学
生物
化学
生物化学
癌症
乳腺癌
作者
Mohammad Z. Haider,Amirhossein Sahebkar,Ali H. Eid
标识
DOI:10.2174/0929867330666230501231528
摘要
Atherosclerosis remains a leading contributor to cardiovascular disease-associated morbidity and mortality. Interestingly, the death rate is higher in men than women from atherosclerosis, and the risk increases for postmenopausal women. This suggested a protective role for estrogen in the cardiovasculature. These effects of estrogen were initially thought to be mediated by the classic estrogen receptors, ER alpha, and beta. However, genetic knockdown of these receptors did not abolish estrogen's vasculoprotective effects suggesting that the other membranous G-protein coupled estrogen receptor, GPER1, maybe the actual mediator. Indeed, in addition to its role in vasotone regulation, this GPER1 appears to play important roles in regulating vascular smooth cell phenotype, a critical player in the onset of atherosclerosis. Moreover, GPER1-selective agonists appear to reduce LDL levels by promoting the expression of LDL receptors as well as potentiating LDL re-uptake in liver cells. Further evidence also show that GPER1 can downregulate Proprotein Convertase Subtilisin/Kexin type 9, leading to suppression of LDL receptor breakdown. Here, we review how selective activation of GPER1 might prevent or suppress atherosclerosis, without the many undesired side effects of the non-selective estrogen.
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