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(Circulation. 2007;116:1214-1216.)
© 2007 American Heart Association, Inc.

Editorial

Increased Endoplasmic Reticulum Stress in Atherosclerotic Plaques Associated With Acute Coronary Syndrome

A Balancing Act Between Plaque Stability and Rupture

Jeffrey G. Dickhout, PhD; Stephen M. Colgan, BSc; árka Lhoták, PhD; Richard C. Austin, PhD

From the Henderson Research Centre and McMaster University, Hamilton, Ontario, Canada.

Correspondence to Richard C. Austin, PhD, Henderson Research Centre, 711 Concession St, Hamilton, Ontario, Canada L8V 1C3. E-mail raustin@thrombosis.hhscr.org

Key Words: Editorials • apoptosis • atherosclerosis • coronary disease • plaque

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

Acute coronary syndrome (ACS) represents a series of indications of sudden cardiac ischemia that involve a variety of causes, including acute myocardial infarction and unstable angina.¹ ACS usually is associated with thrombus formation in the coronary artery or coronary artery vasospasm, resulting in myocardial ischemia.² Thrombus formation may involve platelet adhesion and degranulation on damaged or dysfunctional endothelium overlying the intact or ruptured atherosclerotic plaque, as well as microthrombi.³ Atherosclerotic plaque rupture represents a series of deleterious events linked to the breakdown of the fibrous cap. This process may occur as a result of the increased secretion of matrix metalloproteinases by lesion resident macrophages or enhanced apoptotic cell death within the fibrous cap. However, viable smooth muscle cells (SMCs) within the fibrous cap synthesize interstitial collagen fibers that enhance the structural integrity of the plaque and prevent its rupture.⁴

Article p 1226

SMCs within the vascular wall exist in predominantly 2 phenotypes: a contractile phenotype and a synthetic phenotype. Transformation from the quiescent contractile phenotype to the active synthetic phenotype can be stimulated by the products of coagulation, including platelet-derived growth factors.⁵ Indeed, it has been shown that aortic allografts undergoing atherosclerotic changes first experience endothelial disruption, then SMC activation and proliferation accompanied by increased synthesis of extracellular matrix proteins.⁶ The synthetic SMC phenotype is actively involved in de novo protein synthesis and as such may experience endoplasmic reticulum (ER) stress if the protein folding machinery of the ER is overwhelmed by the demand of newly synthesized proteins.⁷ As a . . . [Full Text of this Article]