Copyright © 2003 by the European Society of Cardiology.
Review article
Angiogenesis: basic pathophysiology and implications for disease
Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK
* Corresponding author. Tel.: +44-121-5075080; fax: +44-121- 554-4083
E-mail address: g.y.h.lip@bham.ac.uk
Received 17 August 2002; revised 26 August 2002; accepted 28 August 2002
Key Words: Angiogenesis • Vasculogenesis • Vascular endothelial growth factor • Fibroblast growth factor • Angiopoietin
| The first 150 words of the full text of this article appear below. |
1. Introduction
The development of new blood vessels is essential to embryonic growth and throughout life for physiological repair processes such as wound healing, post-ischaemic tissue restoration, and the endometrial changes of the menstrual cycle. However, abnormal development of new blood vessels has been implicated in numerous pathophysiological processes. For example, inhibited growth of blood vessels is associated with bowel atresia and peptic ulcers.1–3 Furthermore, although generally focussing on tumour growth, increased vascular growth has been demonstrated in many other non-malignant diseases such rheumatoid arthritis, systemic lupus erythematosus, psoriasis, proliferative retinopathy and atherosclerosis.3–5 It is therefore clear that the subject is currently attracting considerable research energies as tools are becoming available to assess possible therapeutic options.
The formation of the vascular system is fashioned by three processes. During embryogenesis, there is differentiation of embryonic mesenchymal cells (the endothelial precursor cells or angioblasts) into endothelial cells resulting in de novo development of blood
2. Search strategy
3. Basic mechanisms of blood vessel formation
3.1. Vasculogenesis
3.2. Embryonic angiogenesis
3.3. Post-embryonic angiogenesis
4. Angiogenic growth factors
4.1. Fibroblast growth factor
4.1.1. Fibroblastic growth factor-1
4.1.2. Fibroblastic growth factor-2
4.2. Vascular endothelial growth factor
4.2.1. VEGF-A (VEGF)
4.2.2. VEGF-B
4.2.3. VEGF-C
4.2.4. VEGF-D
4.2.5. VEGF-E
4.3. Placenta growth factor
4.4. Angiopoietin
4.5. VEGF receptors
4.5.1. VEGFR-1
4.5.2. VEGFR-2
4.5.3. VEGFR-3
4.5.4. Neuropilins
5. Regulation of VEGF production
5.1. The interaction of VEGF with cytokines and other growth factors
5.2. Effect of oxygen on VEGF expression
5.3. Regulation of VEGF by nitric oxide
5.4. Effect of glucose on VEGF expression
6. Pathophysiological consequences of the interactions between growth factors and their receptors
7. Summary and clinical perspectives
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. D. Ward, B. M. Stone, L. T. Raetzman, and S. A. Camper Cell Proliferation and Vascularization in Mouse Models of Pituitary Hormone Deficiency Mol. Endocrinol., June 1, 2006; 20(6): 1378 - 1390. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. S. Lim, A. D. Blann, A. Y. Chong, B. Freestone, and G. Y.H. Lip Plasma Vascular Endothelial Growth Factor, Angiopoietin-1, and Angiopoietin-2 in Diabetes: Implications for cardiovascular risk and effects of multifactorial intervention Diabetes Care, December 1, 2004; 27(12): 2918 - 2924. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Uchiba, K. Okajima, Y. Oike, Y. Ito, K. Fukudome, H. Isobe, and T. Suda Activated Protein C Induces Endothelial Cell Proliferation by Mitogen-Activated Protein Kinase Activation In Vitro and Angiogenesis In Vivo Circ. Res., July 9, 2004; 95(1): 34 - 41. [Abstract] [Full Text] [PDF]
|
|