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(Circulation Research. 2001;89:563.)
© 2001 American Heart Association, Inc.

Editorial

Smoking-Induced Vascular Disease

A New Twist on an Old Theme

Peter McNamara, Garret A. FitzGerald

From the Center for Experimental Therapeutics (P.M., G.A.F.) and Department of Pharmacology (G.A.F.), University of Pennsylvania.

Correspondence to Garret A. FitzGerald, MD, Department of Pharmacology–153 Johnson Pavilion, University of Pennsylvania School of Medicine, 3620 Hamilton Walk, Philadelphia, PA 19104-6084. E-mail garret@spirit.gcrc.upenn.edu

Key Words: cytochrome P450 • oxidant stress • isoprostanes • NPAS2 • smoking

Polycyclic aromatic hydrocarbons (PAHs) are recognized widely as potential environmental procarcinogens and have attracted their share of attention from both funding agencies and scientists interested in biomedical research. Curiously, their potential relevance to cardiovascular disease, rather than cancer, has stirred less emotion. This imbalance of attention is reflected also in society’s response to that most intimate form of self-pollution with PAHs (and much else), cigarette smoking. While the States have chosen to allocate varying proportions of their Tobacco Settlements to research, cancer tends to dominate the agenda. Yet, tobacco-related cardiovascular disease yields an even more striking burden on the public health than cancer. It has been estimated that cardiovascular morbidity and mortality are increased 4-fold in smokers and by one third in passive smokers.¹ One might think that such daunting figures would prompt advocacy groups, such as the American Heart Association, to lobby vigorously at the State level for an appropriate allocation of the Tobacco Settlements to cardiovascular research.

Our understanding of the mechanisms by which smoking mediates cardiovascular injury and the factors that determine interindividual susceptibility to smoking-induced tissue injury is remarkably limited. In this issue of Circulation Research, Kerzee and Ramos² draw our attention to a mechanism of potential relevance to acceleration of atherogenesis by PAHs, including those in cigarette smoke. The aryl hydrocarbon receptor (Ahr) is a member of the family of basic helix loop helix proteins (bHLHs) that contain PAS domains. This family includes proteins related to differentiation, such as MyoD, the response to hypoxia, . . . [Full Text of this Article]

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