Oxidation of LDL, Atherogenesis, and Apoptosis

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)698-709
Number of pages12
JournalAnnals of the New York Academy of Sciences
Volume1010
DOIs
Publication statusPublished - 2003

Keywords

  • Apoptosis
  • Atherosclerosis
  • Lipoperoxidation
  • Lipoproteins

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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