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Chemical Atherogenesis: Role of Endogenous and Exogenous Poisons in Disease Development
Center for Environmental Health Sciences, Department of Basic Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762, USA
* Author to whom correspondence should be addressed.
Received: 18 November 2013; in revised form: 6 January 2014 / Accepted: 10 January 2014 / Published: 22 January 2014
Abstract: Chemical atherogenesis is an emerging field that describes how environmental pollutants and endogenous toxins perturb critical pathways that regulate lipid metabolism and inflammation, thus injuring cells found within the vessel wall. Despite growing awareness of the role of environmental pollutants in the development of cardiovascular disease, the field of chemical atherogenesis can broadly include both exogenous and endogenous poisons and the study of molecular, biochemical, and cellular pathways that become dysregulated during atherosclerosis. This integrated approach is logical because exogenous and endogenous toxins often share the same mechanism of toxicity. Chemical atherogenesis is a truly integrative discipline because it incorporates concepts from several different fields, including biochemistry, chemical biology, pharmacology, and toxicology. This review will provide an overview of this emerging research area, focusing on cellular and animal models of disease.
Keywords: chemical atherogenesis; endogenous toxins; environmental pollutants; atherosclerosis; carboxylesterases; inflammation; oxidative stress
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MDPI and ACS Style
Ross, M.K.; Matthews, A.T.; Mangum, L.C. Chemical Atherogenesis: Role of Endogenous and Exogenous Poisons in Disease Development. Toxics 2014, 2, 17-34.
Ross MK, Matthews AT, Mangum LC. Chemical Atherogenesis: Role of Endogenous and Exogenous Poisons in Disease Development. Toxics. 2014; 2(1):17-34.
Ross, Matthew K.; Matthews, Anberitha T.; Mangum, Lee C. 2014. "Chemical Atherogenesis: Role of Endogenous and Exogenous Poisons in Disease Development." Toxics 2, no. 1: 17-34.