Evolving concepts of oxidative stress and reactive oxygen species in cardiovascular disease
- PMID: 22956414
- PMCID: PMC3872835
- DOI: 10.1007/s11883-012-0266-8
Evolving concepts of oxidative stress and reactive oxygen species in cardiovascular disease
Abstract
Cardiovascular disease (CVD) continues to be a substantial health-care burden, despite recent treatment advances. Oxidative stress has long been regarded as a key pathophysiological mediator that ultimately leads to CVD including atherosclerosis, hypertension and heart failure. Over the past decade, emerging evidence has shifted our understanding of reactive oxygen species (ROS) from its harmful role to being signaling molecules. Here, we reviewed recent advances in our understanding of ROS that mediate the complex process of CVDs, with a focus on major ROS signaling and sources such as mitochondria and Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidases.
References
-
- Keaney JF, Larson MG, Vasan RS, Wilson PWF, Lipinska I, Corey D, Massaro JM, Sutherland P, Vita JA, Benjamin EJ Framingham Study. Obesity and systemic oxidative stress: clinical correlates of oxidative stress in the Framingham Study. Arterioscler Thromb Vasc Biol. 2003;23:434–439. - PubMed
-
- Rao F, Zhang K, Khandrika S, Mahata M, Fung MM, Ziegler MG, Rana BK, O’Connor DT. Isoprostane, an “intermediate phenotype” for oxidative stress heritability, risk trait associations, and the influence of chromogranin B polymorphism. J Am Coll Cardiol. 2010;56:1338–1350. - PubMed
-
- Lambeth JD. NOX enzymes and the biology of reactive oxygen. Nat Rev Immunol. 2004;4:181–189. - PubMed
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