doi: 10.1161/01.ATV.0000099269.04527.88
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© 2003 American Heart Association, Inc.
Editorials |
Out of Balance
A Role of Impaired Superoxide Dismutase Activity for Vascular Constrictive Remodeling After Angioplasty
From the Institut für Kardiovaskuläre Physiologie, Klinikum der J.W. Goethe-Universität, Theodor-Stern-Kai 7, Frankfurt Germany.
Address correspondence to Ralf P. Brandes, MD, Institut für Kardiovaskuläre Physiologie, Klinikum der J.W. Goethe-Universität, Theodor-Stern-Kai 7, D-60596 Frankfurt am Main, Germany. E-mail r.brandes@em.uni-frankfurt.de
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Lumen loss by constrictive remodeling is a mechanistically still incompletely understood, clinically important problem frequently arising after balloon angioplasty. The arterial trauma, potentially in combination with the destruction of the vascular endothelium, gives rise to a fundamental reorganization of the extracellular matrix. This process is mediated by vascular fibrosis and subsequent condensation of the matrix, ultimately leading to shrinkage of the scar and of the vessel. Several elements contribute to remodeling, including smooth muscle cells and adventitial fibroblasts, resulting in the expression and secretion of matrix proteins such as collagen and of matrix-degrading metalloproteinases (MMPs). Furthermore, cellular proliferation, migration, apoptosis, and vascular spasm are involved in the process.1
See page 2197
Reactive oxygen and nitrogen species play a central role in the regulation of the activity state of vascular cells. Several studies have demonstrated that oxidative as well as nitrosative stress occurs after balloon injury of arteries.2 The pathophysiological role of redox stress for constrictive remodeling, however, is still obscure. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Leite et al3 communicate an elegant study that provides insights into the complicated interplay of reactive oxygen and nitrogen species after balloon angioplasty finally leading to constrictive remodeling. Their observation of an attenuation of vascular superoxide dismutase (SOD) activity after angioplasty in conjunction with the demonstration that delayed systemic application of extracellular SOD (ecSOD) prevents vascular shrinkage after angioplasty is intriguing and could give rise to a reassessment of our current doctrines of angioplasty-induced redox stress.
SOD, as the only