Abstract
Pharmacological agents directed against the integrins alpha(v)beta(3) and alpha(v)beta(5) have been reported to inhibit angiogenesis. However, genetic ablations of the genes encoding these integrins fail to block angiogenesis and in some cases even enhance it. This apparent paradox suggests the hypotheses that these integrins are negative regulators of angiogenesis and that the drugs targeting them may be acting as agonists rather than antagonists.
MeSH terms
-
Animals
-
Antibodies, Monoclonal / pharmacology
-
Antibodies, Monoclonal, Humanized
-
Apoptosis / physiology
-
Autoantigens / pharmacology
-
Collagen Type IV / pharmacology
-
Humans
-
Integrins / drug effects*
-
Integrins / genetics
-
Integrins / metabolism*
-
Neovascularization, Pathologic / drug therapy*
-
Neovascularization, Physiologic / drug effects
-
Neovascularization, Physiologic / physiology*
-
Receptors, Vitronectin / drug effects
-
Receptors, Vitronectin / genetics
-
Receptors, Vitronectin / metabolism
Substances
-
Antibodies, Monoclonal
-
Antibodies, Monoclonal, Humanized
-
Autoantigens
-
Collagen Type IV
-
Integrins
-
Receptors, Vitronectin
-
integrin alphaVbeta5
-
type IV collagen alpha3 chain
-
etaracizumab