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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 536962, 25 pages
Review Article

NSAIDs and Cardiovascular Diseases: Role of Reactive Oxygen Species

1Department of Neurobiology, Physiology, and Behavior, University of California, Davis, CA 95616, USA
2Department of Physiology and Membrane Biology, University of California, Davis, CA 95616, USA

Received 22 December 2014; Revised 3 March 2015; Accepted 3 March 2015

Academic Editor: Mark J. Crabtree

Copyright © 2015 Rajeshwary Ghosh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly used drugs worldwide. NSAIDs are used for a variety of conditions including pain, rheumatoid arthritis, and musculoskeletal disorders. The beneficial effects of NSAIDs in reducing or relieving pain are well established, and other benefits such as reducing inflammation and anticancer effects are also documented. The undesirable side effects of NSAIDs include ulcers, internal bleeding, kidney failure, and increased risk of heart attack and stroke. Some of these side effects may be due to the oxidative stress induced by NSAIDs in different tissues. NSAIDs have been shown to induce reactive oxygen species (ROS) in different cell types including cardiac and cardiovascular related cells. Increases in ROS result in increased levels of oxidized proteins which alters key intracellular signaling pathways. One of these key pathways is apoptosis which causes cell death when significantly activated. This review discusses the relationship between NSAIDs and cardiovascular diseases (CVD) and the role of NSAID-induced ROS in CVD.