(Circulation. 2008;117:3168-3170.)
© 2008 American Heart Association, Inc.
Editorial |
From the Donald W. Reynolds Cardiovascular Clinical Research Center, Cardiovascular Division, Department of Medicine, Brigham and Womens Hospital, Harvard Medical School, Boston, Mass (P.L., F.K.S.); Center for Systems Biology, Massachusetts General Hospital, and Harvard Medical School, Boston, Mass (M.N., M.J.P.); and Center for Molecular Imaging Research, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Mass (M.N., M.J.P., F.K.S.).
Correspondence to Peter Libby, MD, 77 Ave Louis Pasteur, NRB7, Boston, MA 02115. E-mail: plibby@rics.bwh.harvard.edu
Key Words: Editorials endothelium atherosclerosis plaque
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The atherosclerotic plaque typically harbors cells of several lineages whose conversations, mediated by extracellular or cell surface–associated messengers, influence decisively the biology and clinical consequences of the lesion. Early vascular biology studies defined the resting state of the endothelium, characterized by the elaboration of antithrombotic and vasodilatory mediators. The activated endothelium recruits inflammatory leukocytes, favors clot accumulation, participates in angiogenesis, and can influence the behavior of subjacent smooth muscle cells in ways that favor atherogenesis and vasoconstriction (Figure). More recently, we have come to appreciate that the endothelial cell not only can exhibit a spectrum of functions, but that some may arise postnatally from bone marrow–derived precursors.1 Thus, the heterogeneity of endothelial cells depends not only on the mutability of their function but also on their origin. The diversity of endothelium depends not only on lineage but also location, with increasingly well-understood differences between arterial, microvascular, and venous endothelial cells.
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