Loss of bone marrow-derived vascular progenitor cells leads to inflammation and atherosclerosis.

BACKGROUND Aging represents the most powerful risk for the development of atherosclerosis and atherosclerotic thromboembolic complications. Yet, the mechanism by which aging affects the arterial wall and its deterioration has remained essentially uncharacterized. FINDINGS Chronic injuries to the arterial wall contribute to the development of atherosclerosis. However, it is important to note that a complex repair system that involves both local and bone marrow-derived cells maintains arterial homeostasis and integrity. With this review, we explain how the age-dependent failure of the bone marrow to produce vascular progenitor cells responsible for such arterial repair--an inability that results from the impact of a lifetime of risk factors such as hyperlipidemia--drives atherosclerosis and its thromboembolic complications. As a consequence of such failure, the normal processes of arterial wall repair and rejuvenation are impaired. The disequilibrium that ensues between injury of the arterial wall and repair leads to atherosclerotic inflammation and consequent thromboembolic complications. CONCLUSION The bone marrow and derived progenitor cells represent key regulators of atherosclerosis, and progress in the prevention and treatment of atherosclerosis and its thromboembolic complications will need to take into account this new dimension for the disease process.

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