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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1509.)
© 2002 American Heart Association, Inc.

Editorials

Re-endothelialization Via Bone Marrow-Derived Progenitor Cells

Still Another Target of Statins in Vascular Disease

Johan Thyberg

From the Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.

Correspondence to Johan Thyberg, Department of Cell and Molecular Biology, Karolinska Institutet, Box 285, S-17177 Stockholm Sweden. E-mail johan.thyberg@cmb.ki.se

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

According to the response to injury hypothesis presented by Ross and Glomset¹ more than 25 years ago, the formation of atherosclerotic plaques is the result of damage to the endothelium. The key steps in this process are: (1) a physical or chemical disruption of the endothelial cell (EC) barrier; (2) platelet adhesion to exposed subendothelial matrix and platelet degranulation; (3) movement of leukocytes (primarily monocytes and T lymphocytes) and plasma constituents into the arterial intima; (4) migration of smooth muscle cells (SMCs) from the media to the intima; and (5) growth in size of the intimal lesions by cell proliferation, deposition of extracellular matrix components, and lipid accumulation (Figure 1). The original model has later been modified continually, among other reasons, to stress that the endothelial damage may have the nature of a functional disturbance rather than a real detachment. This also implies that the relative importance of the above-mentioned steps may differ in different situations.^2–4 Nevertheless, the basic concept is still largely the same, and as long as the injurious influence remains, the process will continue and lead to formation of complicated lesions, eventually causing complications such as heart and brain infarction. If, on the other hand, the factors causing a harmful effect on the inner lining of the arteries are removed (eg, hypertension, hyperlipidemia, and smoking), the physical and/or functional integrity of the endothelial cell layer may be restored and the disease halted. An important object in the treatment and prevention of atherosclerosis and other related . . . [Full Text of this Article]

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