O ver the last several years, the idea that inflammation plays a key role in atherosclerosis and its complications has received considerable attention.1 Inflammatory cell infiltration is observed in atherosclerotic plaques at virtually all stages, from the fatty streak to the advanced atheromatous lesions with plaque disruption and thrombosis.1,2 Atherosclerosis is substantially prevented when the biological effects of genes critical for the initiation or maintenance of inflammatory cell recruitment, survival, proliferation, and activation, such as monocyte chemotactic protein-1, interleukin-8, and macrophage colony stimulating factor, are eliminated by gene knockout in atherosclerosis-prone dyslipidemic mice.[3][4][5] Similarly, the inhibition of inflammatory signaling pathways mediated by the ligation of CD-40 also results in reduced atherosclerosis in mice.
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Prediman K. Shah (2000) studied this question.
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