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By S. Parthasarathy

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2002), with some individuals demonstrating unique resistance. 25 mg/dL (Khosla & Sundram, 1996). Approximately 60% of plasma LDL in hamsters is removed by hepatic receptors. 6 mg/hour 32 Atherogenesis (Suckling & Jackson, 1993). However, the fact that hamsters and humans share a common LDL clearance mechanism makes the hamster a suitable model for this aspect of cholesterol metabolism. Hamsters and humans also share CETP molecules (Suckling & Jackson, 1993) that transfer the cholesterol component of LDL to HDL, a key step in reverse cholesterol transport.

Maeda N. (1992) Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science, 258, 468-471. Zhao L. D. (2004) Lipoxygenase pathways in atherogenesis. Trends Cardiovasc Med, 14, 191-195. J. D. (2004) The 5-lipoxygenase pathway promotes pathogenesis of hyperlipidemia dependent aortic aneurysm. Nat Med, 10, 966-973. K. (2000) Transfer of CD4(+) T cells aggravates atherosclerosis in immunodeficient apolipoprotein E knockout mice. Circulation, 102, 2919-2922. 2 Spontaneous Atherosclerosis in Pigeons: A Good Model of Human Disease J.

1992;). 2 Atherogenesis risk factors Major physiological conditions such as high blood cholesterol, high blood pressure, diabetes, a skewed lipoprotein profile, heredity, advanced age, and maleness can increase an Spontaneous Atherosclerosis in Pigeons: A Good Model of Human Disease 27 individual’s chance of developing atherosclerosis. Collectively, these risk factors, along with lifestyle patterns such as physical inactivity, smoking, obesity, and stress have been statistically correlated with specific stages of lesion development, plaque stability, and overall disease outcome in the general population.

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