QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wilcox, J. N. Articles by Blumenthal, B. F. Search for Related Content PubMed PubMed Citation Articles by Wilcox, J. N. Articles by Blumenthal, B. F.

Thrombotic Mechanisms in Atherosclerosis: Potential Impact of Soy Proteins¹

Josiah N. Wilcox^*,2 and Barbara F. Blumenthal

^* Division of Hematology and Oncology, Department of Medicine, Emory University, Atlanta, GA 30322 Nutritional Consulting Associates, PO Box 22, Ansonia, CT 06401

Generally injuries that remove or disrupt the endothelial cells lining blood vessels stimulate formation of vascular lesions composed of smooth muscle cells. One of the first events after such endothelial cell disruption is the generation of thrombin at the site of injury. This leads to platelet activation and thrombus formation. Evidence suggests that thrombus formation may stimulate smooth muscle-cell proliferation through the action of any number of factors emanating from the thrombus including platelet- or macrophage-derived factors, platelet-derived growth factor, basic fibroblast growth factor or thrombin. Atherosclerotic plaques continue to grow for many years. The slow indolent process of nondenuding chemical injury of the endothelium and lesion formation may be accelerated periodically by thrombi forming on the lumenal surface at sites of small denuding injuries leading to progressive atherosclerotic disease. Genistein, an isoflavonoid derived from soy products, has been shown to inhibit thrombin formation and platelet activation in vitro in addition to its antigrowth factor activity. Should it have similar actions in vivo, this compound has the potential to affect the progression of atherosclerotic disease by modifying coagulation responses. To assess the potential of genistein as a therapeutic for vascular disease, additional studies will be required to establish its effect on experimental vascular lesion formation.

KEY WORDS: • atherosclerosis • genistein • vascular lesion • isoflavonoid

¹ Presented at the First International Symposium on the Role of Soy in Preventing and Treating Chronic Disease, held in Mesa, AZ, February 20–23, 1994. The symposium was sponsored by Protein Technologies International, the soybean growers from Nebraska, Indiana and Iowa and the United Soybean Board. Guest editors for this symposium were Mark Messina, 1543 Lincoln Street, Port Townsend, WA 98368, and John W. Erdman, Jr., Division of Nutritional Sciences, University of Illinois, Urbana, IL 61801-3852. Supported by NIH HL47838-01.

² To whom correspondence should be addressed: Division of Hematology and Oncology, Department of Medicine, Emory University, Drawer AJ, Atlanta, GA 30322.