PMID- 11036931
OWN - NLM
STAT- MEDLINE
DCOM- 20001113
LR  - 20220409
IS  - 0079-9963 (Print)
IS  - 0079-9963 (Linking)
VI  - 55
DP  - 2000
TI  - Vascular endothelial growth factor and the regulation of angiogenesis.
PG  - 15-35; discussion 35-6
AB  - The development of a vascular supply is essential not only for organ development 
      and differentiation during embryogenesis but also for wound healing and 
      reproductive functions in the adult Folkman, 1995). Angiogenesis is also 
      implicated in the pathogenesis of a variety of disorders: proliferative 
      retinopathies, age-related macular degeneration, tumors, rheumatoid arthritis, 
      and psoriasis (Folkman, 1995; Garner, 1994). Several potential regulators of 
      angiogenesis have been identified, including fibroblast growth factor-a (aFGF), 
      bFGF, transforming growth factor-alpha (TGF-alpha), TGF-beta, hepatocyte growth 
      factor/scatter factor (HGF/SF), tumor necrosis factor-alpha (TNF-alpha), 
      angiogenin, and interleukin-8 (IL-8) (Folkman and Shing, 1992; Risau, 1997). More 
      recently, the angiopoietins, the ligands of the Tie-2 receptor (Suri et al., 
      1996; Maisonpierre et al., 1997), have been identified. Vascular endothelial 
      growth factor (VEGF) is an endothelial-cell-specific mitogen. The finding that 
      VEGF was potent and specific for vascular endothelial cells and, unlike bFGF, 
      freely diffusible, led to the hypothesis that this molecule plays a unique role 
      in the regulation of physiological and pathological angiogenesis (Ferrara and 
      Henzel, 1989: Leung et al., 1989). Over the last few years, several additional 
      members of the VEGF gene family have been identified, including placenta growth 
      factor (PIGF) (Maglione et al., 1991,1993), VEGF-B (Olofsson et al., 1996), 
      VEGF-C (Joukov et al., 1996; Lee et al., 1996), and VEGF-D (Orlandini et al., 
      1996. Achen et al., 1998). There is compelling evidence that VEGF plays an 
      essential role in the development and differentiation of the cardiovascular 
      system (Ferrara and Davis-Smyth, 1997).
FAU - Ferrara, N
AU  - Ferrara N
AD  - Department of Molecular Oncology, Genentech, Inc., South San Francisco, 
      Caliofornia 94080, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Recent Prog Horm Res
JT  - Recent progress in hormone research
JID - 0404471
RN  - 0 (Endothelial Growth Factors)
RN  - 0 (Growth Substances)
RN  - 0 (Lymphokines)
RN  - 0 (Receptors, Growth Factor)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (Vascular Endothelial Growth Factors)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Cell Differentiation
MH  - Cell Transformation, Neoplastic
MH  - Endothelial Growth Factors/genetics/*physiology
MH  - Female
MH  - Gene Expression Regulation
MH  - Growth Substances/physiology
MH  - Humans
MH  - Lymphokines/genetics/*physiology
MH  - Neovascularization, Pathologic
MH  - *Neovascularization, Physiologic
MH  - Oxygen/metabolism
MH  - Receptor Protein-Tyrosine Kinases/physiology
MH  - Receptors, Growth Factor/physiology
MH  - Receptors, Vascular Endothelial Growth Factor
MH  - Signal Transduction
MH  - Vascular Endothelial Growth Factor A
MH  - Vascular Endothelial Growth Factors
RF  - 180
EDAT- 2000/10/19 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/10/19 11:00
PHST- 2000/10/19 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/10/19 11:00 [entrez]
PST - ppublish
SO  - Recent Prog Horm Res. 2000;55:15-35; discussion 35-6.