Role of eNOS in neovascularization: NO for endothelial progenitor cells

被引：216

作者：

Duda, DG ^{[1
]}

Fukumura, D ^{[1
]}

Jain, RK ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Dept Radiat Oncol, EL Steele Lab Tumor Biol, Boston, MA 02114 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2004年 / 10卷 / 04期

关键词：

D O I：

10.1016/j.molmed.2004.02.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Nitric oxide (NO) is a gaseous molecule with an astonishingly wide range of physiological and pathophysiological activities, including the regulation of vessel tone and angiogenesis in wound healing, inflammation, ischaemic cardiovascular diseases and malignant diseases. Recent data have revealed the predominant role of endothelial nitric oxide synthase (eNOS), an endothelial-cell-specific isoform of NO producing enzyme, in both angiogenesis (the development of new blood vessels derived from existing vessels) and vasculogenesis (blood vessel formation de novo from progenitor cells). In addition, successes in gene therapy, together with the recent development of an eNOS-specific inhibitor, suggest that the modulation of eNOS might be a potent new strategy for the control of pathological neovascularization.

引用

页码：143 / 145

页数：3

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