**1. Introduction**

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This review describes theories of human atherogenesis and experimental results evaluating gene or protein expression in the pigeon model for spontaneous atherosclerosis. The spontane‐ ous disease in the pigeon differentiates from other animal models that require manipulation (genetic, nutritional, environmental) to induce the disease state. Both susceptible and resistant pigeons have been studied with susceptibility being inherited as an autosomal recessive trait. The aims are to present the pigeon data in comparison to current theories of the human disease.

Atherosclerotic cardiovascular disease is the leading cause of death in economically devel‐ oped countries. The underlying cause(s) remains unclear despite a variety of hypotheses that have attempted to explain the initiation of atherosclerotic lesions. Many genetic factors that contribute to lesion progression and the probability of plaque rupture have been identi‐ fied in the general population. All forms of heart disease have a strong familial component. However, little is known about the specific genes that determine disease predisposition or how such genes interact with each other and the environment to initiate foam cell formation in any one individual. Numerous, complex gene-environment interactions are believed to be involved in the disease [1] and "although there has been considerable success in identifying genes for the rare disorders associated with atherosclerosis, the understanding of genes in‐ volved in the more common forms is largely incomplete" [2]. New molecular markers need to be developed in order to identify susceptible individuals *prior to* the appearance of clinical symptoms. Until the heritable component of atherosclerosis susceptibility is understood, correlation of various risk factors with specific metabolic or pathological features will be dif‐ ficult to assess, and prevention efforts will remain equivocal.

© 2013 Anderson et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
