Special Article |
From the Division of Cardiology, Department of Medicine (F.P., L.L.D., A.G.), Physiological Science (A.G), and Physiology (L.L.D.), UCLA School of Medicine, Los Angeles, Calif.
Correspondence to Linda L. Demer, MD, PhD, Chief, Division of Cardiology, 10833 Le Conte Avenue, Center for the Health Sciences 47-123, Los Angeles, CA 90095-1679. E-mail ldemer{at}mednet.ucla.edu
Abstract
AbstractCardiovascular disease and osteoporosis together account for most of the morbidity and mortality in our aging population despite significant improvements in treatment. Recently, converging lines of evidence suggest that these 2 diseases share an etiologic factor that hyperlipidemia contributes not only to atherosclerotic plaque formation, but also to osteoporosis, following a similar biologic mechanism involving lipid oxidation. In vitro studies indicate that lipid products of oxidation promote osteoblastic differentiation of vascular cells and inhibit such differentiation in bone cells. Ex vivo, in vivo, and clinical studies further suggest that lipid-lowering agents reduce both atherosclerotic calcification and osteoporosis. Whether lipid-lowering agents reduce osteoporosis directly or indirectly through lipid reduction remains controversial.
Key Words: atherosclerosis osteoporosis calcification
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