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(Hypertension. 2008;51:175.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Angiotensin II

One Driving Force Behind Atherogenesis

Cornelius F.H. Mueller; Georg Nickenig

From Medizinische Klinik und Poliklinik II, Innere Medizin, Universitätsklinikum Bonn, Germany.

Correspondence to Cornelius Mueller, Medizinische Klinik und Poliklinik II, Universitätsklinikum Bonn, Sigmund Freud Str. 25, 53105 Bonn, Germany. E-mail cornelius.mueller@ukb.uni-bonn.de

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

Investigating the mechanisms of atherosclerosis, the number one cause of death in the civilized world, is an arduous task. During the last 5 decades, many aspects of atherosclerotic lesion development have been revealed and many hypotheses have been tested. Thanks to this gigantic effort, our knowledge of vascular biology and engaged pathogenic mechanisms have grown enormously. In spite of all this work, time, and money spent in thousands of laboratories all over the world, atherosclerosis remains something of an unsolved mystery. Every problem solved and every question answered raises even more questions and debates. This is largely because of the fact that there is not one single factor driving atherogenesis but many. However, there are some factors which have remained on stage for many years and from which a considerable part of the scientific community is willing to claim that these players deserve long-term attention. Among these, angiotensin II has been recognized as a major driving force behind endothelial dysfunction and atherosclerotic plaque development. Supposedly, generation of reactive oxygen species,¹ activation of proapoptotic pathways, vascular smooth muscle cell (VSMC) proliferation,^2,3 proinflammation,⁴ enhanced endothelial degeneration,⁵ and reduced vascular regeneration⁶ resemble mechanisms underlying the proatherosclerotic properties of angiotensin II.

In the present issue of Hypertension, Weiss and Taylor investigated a low renin model of hypertension and present data which underline the key role of angiotensin II in atherogenesis.⁷ deoxycorticosterone acetate (DOCA) salt induced hypertension is an often used model. What makes this model unique is the fact that DOCA salt induced . . . [Full Text of this Article]

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Deoxycorticosterone Acetate Salt Hypertension in Apolipoprotein E^–/– Mice Results in Accelerated Atherosclerosis: The Role of Angiotensin II

Daiana Weiss and W. Robert Taylor
Hypertension 2008 51: 218-224. [Abstract] [Full Text] [PDF]

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