Abstract
Nicotinic acetylcholine receptors (nAChRs) were first described in non-excitable cells just more than a decade ago. The nAChRs on endothelial cells modulate key angiogenic processes, including endothelial cell survival, proliferation, and migration. The receptors may be stimulated by endogenous agonists such as acetylcholine, or exogenous chemicals such as nicotine, to activate physiologic angiogenesis (such as in wound healing) or pathologic angiogenesis (such as retinal neovascularization or tumor angiogenesis). The endothelial nAChRs may represent a target for therapeutic modulation of disorders characterized by insufficient or pathologic angiogenesis.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Acetylcholine / pharmacology
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Angiogenesis Inhibitors / pharmacology
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Angiogenesis Inhibitors / therapeutic use
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Cholinergic Agents / pharmacology
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Endothelial Cells / metabolism
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Endothelium, Vascular / metabolism*
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Endothelium, Vascular / physiopathology
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Humans
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Neovascularization, Pathologic*
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Neovascularization, Physiologic*
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Nicotine / pharmacology
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Nicotinic Agonists / pharmacology
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Nitric Oxide Synthase Type III / metabolism
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Receptors, Nicotinic / drug effects
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Receptors, Nicotinic / metabolism*
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Vascular Endothelial Growth Factor A
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Wound Healing
Substances
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Angiogenesis Inhibitors
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Cholinergic Agents
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Nicotinic Agonists
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Receptors, Nicotinic
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Vascular Endothelial Growth Factor A
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Nicotine
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NOS3 protein, human
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Nitric Oxide Synthase Type III
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Acetylcholine