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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1088.)
© 2005 American Heart Association, Inc.

Editorials

CD40 Ligand

Not Bad to the Bone (Marrow), After All

Olujimi A. Ajijola; Pascal J. Goldschmidt-Clermont; Lisa L. Satterwhite

From the Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC.

Correspondence to Pascal J. Goldschmidt-Clermont, Division of Cardiology, Department of Medicine, Duke University Medical Center, DUMC 3703, Durham, NC 27710. E-mail Golds017@mc.duke.edu

Key Words: atherosclerosis • inflammation • CD40 ligand • stem cells • endothelial progenitor cells

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Atherosclerosis is a chronic inflammatory process that affects arteries selectively and results from imbalance between injury and repair. The complex etiology of atherosclerosis has proved formidable, indeed.^1,2 Although linked to the presence of microorganisms, the atherosclerotic inflammation does not seem to result from infection; specifically, not the type of infection that can be treated with adequate antibiotics.^3,4 Infections can nevertheless promote atherosclerotic inflammation indirectly by augmenting the release of cytokines in the bloodstream, such that local arterial intimal lesions can be affected.⁵ Furthermore, some antiinflammatory drugs like COX-2 inhibitors appear to worsen the risk of patients for cardiac events, rather than antagonize atherosclerotic inflammation and its thromboembolic consequences.^6,7 Hence, the development of vascular specific antiinflammatory therapies is limited by the necessity of a basal inflammatory response to maintain arterial homeostasis by constitutive arterial repair involving both local and distant processes, such as the production of vascular precursor cells by the bone marrow. There is an exquisite need for selective antiinflammatory drugs, drugs that do not alter the limited form of inflammation required for arterial repair signaling but do control the unchecked inflammation that occurs in patients who are unable, for a variety of reasons, to mount a successful repair response.

See page 1244

In such context, the dyad of CD40 and its extracellular ligand (CD40L, also called CD154) appears an ideal target for more specific antiatherosclerotic therapies. The proinflammatory dyad (CD40/CD40L) is expressed on the surface of endothelial and smooth muscle cells, macrophages, lymphocytes, megakaryocytes, and platelets—all progeny of bone . . . [Full Text of this Article]

Related Article:

Atherogenesis in Mice Does Not Require CD40 Ligand From Bone Marrow–Derived Cells

Udo Bavendiek, Andreas Zirlik, Samantha LaClair, Lindsey MacFarlane, Peter Libby, and Uwe Schönbeck
Arterioscler Thromb Vasc Biol 2005 25: 1244-1249. [Abstract] [Full Text] [PDF]