期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 106, 期 1, 页码 333-337出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.91360.2008
关键词
estrogen receptor; endothelial nitric oxide synthase
资金
- Ministero del Lavoro, della Salute e delle Politiche Sociali
- Association Francaise contre les Myopathies [MNM2-06]
- Muscular Dystrophy Association (MDA) [88202]
- Fondo per gli investimenti della Ricerca di Base (FIRB) [RBLA035A4X-1FIRB]
- UE FP6 [UE-LHSB-CT-04-502988, DdT2-06]
Farsetti A, Grasselli A, Bacchetti S, Gaetano C, Capogrossi MC. The telomerase tale in vascular aging: regulation by estrogens and nitric oxide signaling. J Appl Physiol 106: 333-337, 2009. First published November 20, 2008; doi:10.1152/japplphysiol.91360.2008.-Hormones and nitric oxide (NO), a free radical, are ancestral molecules, conserved through evolution, that modulate many aspects of the physiology and pathophysiology of living organisms by regulating transcription of genes involved in development, metabolism, and differentiation. Of interest, both estrogen and NO signaling, specifically through the estrogen receptor-alpha (ER alpha) and the endothelial isoform of the nitric oxide synthase (eNOS), have been shown to counteract endothelial senescence through a shared downstream effector, the catalytic subunit of human telomerase (hTERT), a key molecule in the aging process. Since aging is the first and most relevant risk factor in cardiovascular diseases, it is tempting to speculate that hTERT may be at the cross point between the NO and estrogen pathways. The present review will focus on the evolutionary and molecular aspects linking eNOS, ERs, and hTERT in counteracting the process of endothelial cell aging.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据