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(Circulation. 2006;114:870-872.)
© 2006 American Heart Association, Inc.

Editorial

The Heat Is on

Heat-Shock Proteins and Atherosclerosis

Georg Wick, MD

From the Division of Experimental Pathophysiology and Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

Correspondence to Georg Wick, MD, Division of Experimental Pathophysiology and Immunology, Biocenter, Medical University of Innsbruck, Fritz-Pregl-Strasse 3/IV, A-6020 Innsbruck, Austria. E-mail Georg.Wick@i-med.ac.at

Key Words: Editorials • atherosclerosis • heat-shock proteins • inflammation

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

It is common knowledge that atherosclerosis is a multifactorial disease, and the disease-promoting role of classic risk factors for atherosclerosis, such as high serum cholesterol levels, diabetes, hypertension, smoking, and various types of infections, has been proven in innumerable clinical studies. Despite the fact that we are dealing with a chronic disease, however, there is a surprising scarcity of reports dealing with the very first stages of atherogenesis, ie, those that are not yet leading to clinical symptoms. It is now evident that inflammatory/immunologic processes play a major role in the development of atherosclerosis. The correlation between the presence and amount of inflammatory surrogate markers and the occurrence of sonographically demonstrable early arterial changes becomes more significant the earlier in the course of the disease that these analyses are performed. Although complicated atherosclerotic lesions, as the name implies, are composed of many different cellular and extracellular constituents, the earliest lesions are characterized by intimal infiltration by mononuclear cells often still without the presence of foam cells, especially in those instances in which risk factors other than high serum cholesterol levels are operative. In this context, it is important to remember that the first intima-infiltrating cells in early, clinically nonapparent lesions are lymphoid cells, followed by blood-borne monocytes, and finally smooth muscle cells immigrating from the media.¹ Later, both the scavenger receptor–expressing macrophages and smooth muscle cells may transform into foam cells accompanied by fibroblast and myofibroblast proliferation with collagenous and noncollagenous extracellular matrix protein deposition leading to the paradigmatic hardening . . . [Full Text of this Article]

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				M. L. Rose and M. J. Dunn Letter by Rose and Dunn Regarding Article, "Expression of Heat Shock Protein 27 in Human Atherosclerotic Plaques and Increased Plasma Level of Heat Shock Protein 27 in Patients With Acute Coronary Syndrome" Circulation, May 1, 2007; 115(17): e434 - e434. [Full Text] [PDF]