doi: 10.1161/01.RES.0000208078.53239.53
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© 2006 American Heart Association, Inc.
Editorials |
Novel Faces to Old Friends
A Central Role of Inducible NO Synthase for Progenitor Cell Recruitment and a New Antiinflammatory Mechanisms of Statins
From the Institut für Kardiovaskuläre Physiologie, Fachbereich Medizin der J.W. Goethe-Universität, Frankfurt am Main, Germany.
Correspondence to Ralf P. Brandes, Institut für Kardiovaskuläre Physiologie, Fachbereich Medizin der J.W. Goethe-Universität, Theodor-Stern-Kai 7, D-60596 Frankfurt am Main, Germany. E-mail r.brandes@em.uni-frankfurt.de
See related articles, pages 361–369 and 412–420
Key Words: progenitor cells • PPAR • statins
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Coronary artery bypass grafting (CABG) is performed using autologous vein and arterial grafts. Patency rates of arterial grafts are significantly higher than those of vein grafts.1,2 Early vein graft occlusion occurs in up to 12%, potentially attributable to graft thrombosis. The subsequent occlusion rate is 2% to 4% per year, and this problem has been attributed to accelerated vein graft arteriosclerosis,3 a process preceded by intimal hyperplasia that occurs in the first year after implantation. The neointima that forms consists largely of cells expressing smooth muscle markers which are derived in part from circulating progenitor cells (CPC).4
In animal vein graft models, massive endothelial cell apoptosis has been observed during the first weeks after implantation and endothelial cell loss is thought to promote neointimal hyperplasia. Reendothelialization is usually achieved within 4 weeks after implantation,5 and elegant studies in the mouse indicate that this neo-endothelium consists of former circulating progenitor cells that attach to the arterial lumen and then differentiate into endothelial cells.5,6 Despite this hallmark insight, numerous questions remain unsolved. For example; what are the mechanisms guiding CPCs to the vein graft? From which population of cells do the engrafting CPCs derive? What determines whether an adhering CPC acquires a muscle smooth or endothelial phenotype? And finally, what is the significance of CPC endothelial engraftment for the development of vein graft neointima?
In the present issue of Circulation Research, Mayr et al report a central role for the inducible NO synthase (iNOS) in vein graft reendothelialization by CPC in
Related Article:
via Inhibition of the Protein Kinase C Signaling Pathway
Circ. Res. 2006 98: 361-369.