(Augusta, GA) Vascular disease pertains to the disorders that affect our arteries and veins. For the three most common types of vascular disease --carotid, aortic and peripheral aging is a major risk factor. Recent studies suggest that pathological changes not only predispose the vasculature to disease but also impair compensatory adaptations to various stimuli including shear force and injury. Other studies have demonstrated a progressive increase in oxidative stress, activation of inflammatory mediators, and increasing endothelial dysfunction in both humans and animals.

Yet individuals and certain rodent strains display different degrees of "physiological aging" at a given chronological age--suggesting a genetic component in the aging process. Aging within the vasculature is characterized by remodeling events similar to those observed in atherosclerosis. Although this vascular aging may predispose the vasculature to disease, the mechanistic basis for this remodeling is presently not understood. One approach to understanding the progressive changes that occur in the vasculature during aging is to evaluate gene expression in vessels that display varying degrees of aging/remodeling. Such a comprehensive genetic analysis would identify specific molecules involved in the aging process. From this analysis novel pathways that regulate the vascular pathologies that develop with aging could be identified as well as potential markers of vascular aging.

A New Study

Against this backdrop a team of researchers has undertaken a study to identify specific molecules whose genetic regulation is altered during aging and that contribute to age-dependent vascular remodeling. Their results are consistent with the current concept that atherosclerosis is an inflammatory process, and suggests that the Fisher 344/Brown Norway F1 hybrid rat (F344xBNrats) may be a good model for studying the vascular changes that occur early in the development of athe
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
30-Sep-2003

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