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Curr Atheroscler Rep. 2012 Oct;14(5):476-83. doi: 10.1007/s11883-012-0266-8.

Evolving concepts of oxidative stress and reactive oxygen species in cardiovascular disease.

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  • 1Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, 55 Lake Avenue N., S3-851, Worcester, MA 01655, USA. Kai.Chen@umassmed.edu

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.

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