Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions

By Peter Carmeliet, L. Moons, A. Luttun, V. Vincenti, V. Compernolle, M. D. Mol, Wusheng Yan, F. Bono, L. Devy, H. Beck and 19 more. Nature Medicine, 2001

1,746 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/82626729cf063a9ce8c7104aad9d16d72403c899

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

Vascular Endothelial Growth Factor (VEGF) and Its Receptor (VEGFR) Signaling in Angiogenesis: A Crucial Target for Anti- and Pro-Angiogenic Therapies. (2011, background): “However, under pathological conditions, synergism between PlGF and VEGF-A has been shown to contribute to angiogenesis.(16) VEGF-B–/– mice have the phenotype of an atrial conduction defect.”
Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels. (2007, methodology): “Received: March 22, 2007 Revised: July 12, 2007 Accepted: August 10, 2007 Published: November 1, 2007”
Signal transduction by vascular endothelial growth factor receptors. (2012, background): “PlGF is also dispensable for embryonic and adult physiological angiogenesis (Carmeliet et al. 2001), but promotes pathological angiogenesis in a number of diseases (see Fischer et al. 2008 for a more detailed review on the properties of PlGF).”
The roles of vascular endothelial growth factor in bone repair and regeneration (2016, background): “VEGF-C and -D are important for lymphangiogenesis [16, 17]; VEGF-B has a role in embryonic angiogenesis [18] and PlGF is a critical component of pathological angiogenesis [19].”
Vascular endothelial growth factor (VEGF) signaling in tumor progression. (2007, background): “PlGF null mice are viable nd fertile, but they exhibit diminished vascularization of the etina and the corpus luteum [109].”
Regulation of wound healing by growth factors and cytokines. (2003, background): “This upregulation appears to be of functional importance, since PLGF knockout mice were characterized by impaired wound healing as a result of a defect in angiogenesis (45).”
Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis. (2004, background): “…BM to Id mutant cidated. mice (Lyden et al., 1999) or placental growth factor null mice The host contribution to tumor progression is reflected by (Carmeliet et al., 2001; Hattori et al., 2002) restored their ability the roles of tumor infiltrating cells, which orchestrate the tumor to form tumor…”
Molecular mechanisms of lymphangiogenesis in health and disease. (2002, background): “Several molecules have been implicated, but members of the VEGF family of growth factors (VEGF, VEGF-B, -C, -D, and PlGF) and their receptors (VEGFR-1, -2, and -3) play critical roles in mediating angiogenic processes (Carmeliet, 2000; Carmeliet et al., 2001; Dvorak, 2000; Ferrara, 2001; Karkkainen ”
ZD6474 inhibits vascular endothelial growth factor signaling, angiogenesis, and tumor growth following oral administration. (2002, background): “cent data suggest that Flt-1 signaling may be of consequence in pathological angiogenesis (51) but potentially only by virtue of its ability to transactivate KDR.”