The biology of VEGF and its receptors

被引：7706

作者：

Ferrara, N ^{[1
]}

Gerber, HP ^{[1
]}

LeCouter, J ^{[1
]}

机构：

[1] Genentech Inc, Dept Mol Oncol, San Francisco, CA 94080 USA

来源：

NATURE MEDICINE | 2003年 / 9卷 / 06期

关键词：

D O I：

10.1038/nm0603-669

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：

Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions. VEGF has also been implicated in pathological angiogenesis associated with tumors, intraocular neovascular disorders and other conditions. The biological effects of VEGF are mediated by two receptor tyrosine kinases (RTKs), VEGFR-1 and VEGFR-2, which differ considerably in signaling properties. Non-signaling co-receptors also modulate VEGF RTK signaling. Currently, several VEGF inhibitors are undergoing clinical testing in several malignancies. VEGF inhibition is also being tested as a strategy for the prevention of angiogenesis, vascular leakage and visual loss in age-related macular degeneration.

引用

页码：669 / 676

页数：8

共 136 条

[1] Inhibition of vascular endothelial growth factor prevents retinal ischemia-associated iris neovascularization in a nonhuman primate [J].

Adamis, AP ;

Shima, DT ;

Tolentino, MJ ;

Gragoudas, ES ;

Ferrara, N ;

Folkman, J ;

DAmore, PA ;

Miller, JW .

ARCHIVES OF OPHTHALMOLOGY, 1996, 114 (01) :66-71

[2]

Adini A, 2002, CANCER RES, V62, P2749

[3] SUPPRESSION OF RETINAL NEOVASCULARIZATION IN-VIVO BY INHIBITION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) USING SOLUBLE VEGF-RECEPTOR CHIMERIC PROTEINS [J].

AIELLO, LP ;

PIERCE, EA ;

FOLEY, ED ;

TAKAGI, H ;

CHEN, H ;

RIDDLE, L ;

FERRARA, N ;

KING, GL ;

SMITH, LEH .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (23) :10457-10461

[4] VASCULAR ENDOTHELIAL GROWTH-FACTOR IN OCULAR FLUID OF PATIENTS WITH DIABETIC-RETINOPATHY AND OTHER RETINAL DISORDERS [J].

AIELLO, LP ;

AVERY, RL ;

ARRIGG, PG ;

KEYT, BA ;

JAMPEL, HD ;

SHAH, ST ;

PASQUALE, LR ;

THIEME, H ;

IWAMOTO, MA ;

PARK, JE ;

NGUYEN, HV ;

AIELLO, LM ;

FERRARA, N ;

KING, GL .

NEW ENGLAND JOURNAL OF MEDICINE, 1994, 331 (22) :1480-1487

[5] Migration of human monocytes in response to vascular endothelial growth factor (VEGF) is mediated via the VEGF receptor flt-1 [J].

Barleon, B ;

Sozzani, S ;

Zhou, D ;

Weich, HA ;

Mantovani, A ;

Marme, D .

BLOOD, 1996, 87 (08) :3336-3343

[6] Vascular endothelial growth factor increases microvascular permeability via a Ca2+-dependent pathway [J].

Bates, DO ;

Curry, FE .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 273 (02) :H687-H694

[7] Mice lacking the vascular endothelial growth factor-B gene (Vegfb) have smaller hearts, dysfunctional coronary vasculature, and impaired recovery from cardiac ischemia [J].

Bellomo, D ;

Headrick, JP ;

Silins, GU ;

Paterson, CA ;

Thomas, PS ;

Gartside, M ;

Mould, A ;

Cahill, MM ;

Tonks, ID ;

Grimmond, SM ;

Townson, S ;

Wells, C ;

Little, M ;

Cummings, MC ;

Hayward, NK ;

Kay, GF .

CIRCULATION RESEARCH, 2000, 86 (02) :E29-E35

[8] Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal [J].

Benjamin, LE ;

Golijanin, D ;

Itin, A ;

Pode, D ;

Keshet, E .

JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (02) :159-165

[9] Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis [J].

Bergers, G ;

Brekken, R ;

McMahon, G ;

Vu, TH ;

Itoh, T ;

Tamaki, K ;

Tanzawa, K ;

Thorpe, P ;

Itohara, S ;

Werb, Z ;

Hanahan, D .

NATURE CELL BIOLOGY, 2000, 2 (10) :737-744

[10]

Broxmeyer HE, 1995, INT J HEMATOL, V62, P203

← 1 2 3 4 5 6 7 8 9 10 →