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Oxidation of LDL, Atherogenesis, and Apoptosis
CLAUDIO NAPOLI
Departments of Medicine and Clinical Pathology, University of Naples, Naples, Italy
Address for correspondence: Claudio Napoli, M.D., Ph.D., Medicine-UN, P.O. Box, Naples 80131, Italy. claunap{at}tin.it
Ann. N.Y. Acad. Sci. 1010: 698-709 (2003).
A plethora of studies in cultured cells have established that oxidized low-density lipoprotein (oxLDL) may enhance arterial apoptosis that involves both mitochondrial and death receptor pathways (Fas/FasL, TNF receptors I and II), thereby activating caspase cascade and other proteases. When apoptosis is inhibited by Bcl-2 overexpression, oxLDL may trigger necrosis through a calcium-dependent pathway. Despite this effort, the pathophysiological relevance of apoptosis in vivo remains to be elucidated. In principle, apoptosis occurring in atherosclerotic areas could be involved in endothelial cell lining defects, necrotic core formation, and plaque rupture or fissuring. This complex pathogenic framework may favor coronary atherothrombotic events. To date, the pathogenic role of apoptosis in thrombosis is attractive, but a solid evidence is still needed. When the precise role of oxLDL in vascular programmed cell death occurring in vivo is clarified, this may aid in the development of novel therapeutic approaches to adverse atherogenesis and its clinical sequelae.
Key Words: lipoproteins • lipoperoxidation • apoptosis • atherosclerosis
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