ABSTRACT
Atherosclerosis is a complex disease characterized by the accumulation of lipids, matrix, inflammatory cells, and smooth muscle cells in the walls of large arteries. This progressive chronic disease is the result of many insults. The natural history in humans typically progresses through a long clinically silent phase of atheroma formation, which is followed much later in life by the emergence of clinical syndromes, such as stroke and myocardial infarction, which are provoked by plaque disruption and thrombosis. In the last several decades our understanding of atherosclerosis has progressed rapidly because of advances in cell biology and molecular mechanisms of gene regulation, the development of experimental animal models amenable to genetic interventions, and numerous clinical studies identifying risk factors and improved therapies that modify the disease in humans. Pathological mechanisms are better characterized for some recognized clinical risk factors such as hypercholesterolemia, but remain incompletely understood for several other risk factors such as diabetes, smoking, hypertension and systemic inflammation.
