| dc.description.abstract | Heterocellular myoendothelial gap junctions (MEGJs) are essential in coordinating and regulating vasomotion. Little is known about their potential role in disease states. We discuss how alteration in the Cx 43:40 expression ratio at the level. of MEGJs may begin a chain of reactions in the arterial wall resulting in an aneurysm formation. In this model, we assumed that aneurysm is a chronic arterial disease associated with medial degeneration and intimal hyperplasia. It also was assumed that MEGJs are composed of Cx43 and Cx40 in different stoichiometry and that the characteristic of a given junction is in the favor of its most abundantly expressed constituent. The hypothesis of Cx 43:40 stoichiometry indicates that impaired MEGJs may play a role in the pathogenesis of arterial aneurysms. Cx43 upregulation and Cx40 downregulation (increased Cx 43:40 stoichiometry) may induce a cascade of inflammatory, electrical, metabolic and proliferative derangements in the arterial watt, which finally lead to the matrix degradation, intimal hyperplasia, endothelial-medial dissociation and loss of endothelium-dependent hyperpolarizing currents, irregular vasomotion, impaired growth factor activation, and arterial sympathetic deprivation. The final consequence of these alterations is aneurysm formation. (c) 2007 Published by Elsevier Ltd. | |
