Regulation of nitric oxide signalling by thrombospondin 1: implications for anti-angiogenic therapies

被引：238

作者：

Isenberg, Jeff S. ^{[1
]}

Martin-Manso, Gema ^{[1
]}

Maxhimer, Justin B. ^{[1
]}

Roberts, David D. ^{[1
]}

机构：

[1] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA

来源：

NATURE REVIEWS CANCER | 2009年 / 9卷 / 03期

基金：

美国国家卫生研究院;

关键词：

ENDOTHELIAL-GROWTH-FACTOR; C-TERMINAL DOMAIN; COLORECTAL LIVER METASTASES; INTEGRIN-ASSOCIATED PROTEIN; ISCHEMIC TISSUE SURVIVAL; SQUAMOUS-CELL CARCINOMA; TUMOR BLOOD-FLOW; IN-VITRO; HEPATOCELLULAR-CARCINOMA; PLASMA THROMBOSPONDIN;

D O I：

10.1038/nrc2561

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

In addition to long-term regulation of angiogenesis, angiogenic growth factor signalling through nitric oxide (NO) acutely controls blood flow and haemostasis. Inhibition of this pathway may account for the hypertensive and pro-thrombotic side effects of the vascular endothelial growth factor antagonists that are currently used for cancer treatment. The first identified endogenous angiogenesis inhibitor, thrombospondin 1, also controls tissue perfusion, haemostasis and radiosensitivity by antagonizing NO signalling. We examine the role of these and other emerging activities of thrombospondin 1 in cancer. Clarifying how endogenous and therapeutic angiogenesis inhibitors regulate vascular NO signalling could facilitate development of more selective inhibitors.

引用

页码：182 / 194

页数：13

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