Oxidation-sensitive mechanisms, vascular apoptosis and atherosclerosis

Filomena De Nigris, Amir Lerman, Louis J. Ignarro, Sharon Williams-Ignarro, Vincenzo Sica, Andrew H. Baker, Lilach O. Lerman, Yong J. Geng, Claudio Napoli

Research output: Contribution to journalReview articlepeer-review

100 Scopus citations


Increased generation of oxidants, resulting from disruption of aerobic metabolism and from respiratory burst, is an essential defense mechanism against pathogens and aberrant cells. However, oxidative stress can also trigger and enhance deregulated apoptosis or programmed cell death, characteristic of atherosclerotic lesions. Oxidation-sensitive mechanisms also modulate cellular signaling pathways that regulate vascular expression of cytokines and growth factors, and influence atherogenesis, in particular when increased levels of plasma lipoproteins provide ample substrate for lipid peroxidation and lead to increased formation of adducts with lipoprotein amino acids. In some cases, increased oxidation and apoptosis in a group of cells might be beneficial for survival and function of other groups of arterial cells. However, overall, oxidation and apoptosis appear to promote the progression of diseased arteries towards a lesion that is vulnerable to rupture, and to give rise to myocardial infarction and ischemic stroke. Recent rapid advances in our understanding of the interactions between oxidative stress, apoptosis and arterial gene regulation suggest that selective interventions targeting these biological functions have great therapeutic potential.

Original languageEnglish (US)
Pages (from-to)351-359
Number of pages9
JournalTrends in Molecular Medicine
Issue number8
StatePublished - Aug 1 2003

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology


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