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STATE-OF-THE-ART PAPER

Promoting Mechanisms of Vascular Health

Circulating Progenitor Cells, Angiogenesis, and Reverse Cholesterol Transport

Pedro R. Moreno, MD^_*, Javier Sanz, MD^_* and Valentin Fuster, MD, PhD^_*,,_*

^_* Zena and Michael A. Wiener Cardiovascular Institute, and the Marie-Josee and Henry R. Kravis Cardiovascular Health Center, The Mount Sinai School of Medicine, New York, New York
The Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain

Manuscript received November 14, 2008; revised manuscript received January 27, 2009, accepted February 6, 2009.

^_* Reprint requests and correspondence: Dr. Valentin Fuster, Mount Sinai School of Medicine, Box 1030, New York, New York 10029 (Email: valentin.fuster{at}mountsinai.org).

To understand and promote vascular health, we must reduce the aggression to the vessel wall and enhance the physiologic mechanisms leading to restoration of vessel wall function. Three main defense mechanisms are responsible for maintaining cardiovascular homeostasis: the regenerative production of endothelial progenitor cells, vessel wall angiogenesis, and macrophage-mediated reverse cholesterol transport. Endothelial progenitor cells can restore vessel wall function and reduce atherosclerosis. In patients with risk factors, high levels of circulating progenitor cells increase event-free survival from cardiovascular events. Mobilization of progenitor cells includes physical and pharmacological approaches, of which exercise and statin therapy have great potential. Angiogenesis is a pivotal defense mechanism to counteract hypoxia and is needed for plaque regression. However, neovessels are susceptible for intraplaque hemorrhage, particularly in diabetes mellitus. In these patients, the haptoglobin 2-2 genotype is the more affected, and may benefit from an antioxidant approach. Finally, the reverse cholesterol transport system is the main mechanism for plaque regression. In addition to high-density lipoprotein cholesterol, apolipoprotein A-I therapies and the promotion of cholesterol efflux from macrophages by the ABCA1 and ABCG1 transporter systems hold great promise and may be available for therapeutic application in the near future.

Key Words: atherosclerosis • endothelium • angiogenesis • regression

Abbreviations and Acronyms   ApoA-I = apolipoprotein A-I   CETP = cholesterol ester transporter protein   CVD = cardiovascular disease   EPC = endothelial progenitor cell   Hb = hemoglobin   HDL = high-density lipoprotein   HDL-C = high-density lipoprotein cholesterol   Hp = haptoglobin

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