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(Circulation. 2007;116:2782-2785.)
© 2007 American Heart Association, Inc.

Editorial

Inflammation Ushers in Calcification

A Cycle of Damage and Protection?

Catherine M. Shanahan, PhD

From the Division of Cardiovascular Medicine, Kings College London, London, United Kingdom.

Correspondence to Catherine M. Shanahan, PhD, Cardiovascular Division, James Black Centre, Kings College London, 125 Coldharbour Ln, London SE5 9NU, UK. E-mail cathy.shanahan@kcl.ac.uk

Key Words: Editorials • atherosclerosis • calcium • imaging • inflammation

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

The layman’s term "hardening of the arteries" is synonymous with vascular disease and describes the ubiquitous calcification of the intima and media of the vessel wall that occurs in atherosclerosis and aging. Vascular calcification measured and quantified by electron beam computer tomography is a powerful predictor of myocardial infarction, vascular complications such as amputation, and all-cause mortality.¹ Despite this fact, calcification has remained a neglected pathology, particularly in the field of atherosclerosis. This neglect is due in part to the controversy surrounding whether calcification is a bystander marker of disease load or acts to induce plaque rupture and thus increase the cardiovascular event rate; it is also due to the long-held belief that vascular calcification is an end-stage dystrophic process and therefore not amenable to manipulation. However, huge progress has been made over the last 10 years in elucidating the cell biological mechanisms underlying vascular calcification.

Article p 2841

Consensus now exists that calcification is a regulated process, orchestrated by vascular smooth muscle cells (VSMCs) and occurring stepwise in a manner analogous to physiological mineralization processes. In the normal vessel wall, VSMCs are protected from calcification by local and circulating proteins such as matrix Gla protein and fetuin-A that act as mineralization inhibitors. However, in response to insults, VSMCs may die by apoptosis and release apoptotic bodies or may be induced by signals and mechanisms that are still not well defined to release matrix vesicles.² These small membrane-bound microparticles have the capacity to concentrate calcium and phosphate to allow crystal . . . [Full Text of this Article]

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