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.