Pharmacologic strategies to target oxidative stress in heart failure

被引:37
作者
Ahmed Z. [1 ]
Wilson Tang W.H. [1 ]
机构
[1] Section of Heart Failure and Cardiac Transplantation Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH 44195, 9500 Euclid Avenue
关键词
Antioxidants; Coenzyme Q<sub>10</sub>; Heart failure; Omega-3 fatty acids; Oxidative stress; Pharmacologic therapy; Reactive oxygen species; Vitamin supplementation; Xanthine oxidase; Xanthine oxidase inhibitors;
D O I
10.1007/s11897-011-0081-5
中图分类号
学科分类号
摘要
Reactive oxygen species (ROS), which are involved in normal physiological functions at low concentrations, can have deleterious effects when produced in excess. Over time, ROS may result in a pathological state of imbalance known as oxidative stress. Oxidative stress has long been implicated in many diseases, and is consistently associated with poor outcomes in heart failure. Most therapies that are currently being used may provide some reduction in oxidative stress, but there is no consensus on the clinical outcomes of various antioxidants. Currently, there are no antioxidant therapies that are being used routinely to specifically target oxi-dative stress in patients with heart failure. This article reviews the current understanding of ROS generation, and the potential for novel pharmacologic strategies to target oxidative stress in heart failure. © 2012 Springer Science+Business Media, LLC.
引用
收藏
页码:14 / 22
页数:8
相关论文
共 83 条
[1]
Roger V.L., Go A.S., Lloyd-Jones D.M., Et al., Heart disease and stroke statistics-2011 update, Circulation, 123, pp. 209-218, (2011)
[2]
Finkel T., Signal transduction by reactive oxygen species in non-phagocytic cells, Journal of Leukocyte Biology, 65, 3, pp. 337-340, (1999)
[3]
Harman D., Aging: A theory based on free radical and radiation chemistry, J Gerontol., 11, pp. 298-300, (1956)
[4]
Sugamura K., Keaney J.J.F., Reactive oxygen species in cardiovascular disease, Free Radical Biology and Medicine., 51, pp. 978-992, (2011)
[5]
Dreher D., Junod A.F., Role of oxygen free radicals in cancer development, Eur J Cancer., 32 A, pp. 30-38, (1996)
[6]
Whaley-Connell A., McCullough P.A., Sowers J.R., The role of oxidative stress in the metabolic syndrome, Rev Cardiovasc Med., 12, pp. 21-29, (2011)
[7]
Facecchia K., Fochesato L.A., Ray S.D., Et al., Oxidative toxicity in neurodegenerative diseases: Role of mitochondrial dysfunction and therapeutic strategies, Journal of Toxicology, (2011)
[8]
Giordano F.J., Oxygen, oxidative stress, hypoxia, and heart failure, Journal of Clinical Investigation, 115, 3, pp. 500-508, (2005)
[9]
Bertrand M.E., Provision of cardiovascular protection by ACE inhibitors: A review of recent trials, Current Medical Research and Opinion, 20, 10, pp. 1559-1569, (2004)
[10]
Ono H., Minatoguchi S., Watanabe K., Yamada Y., Mizukusa T., Kawasaki H., Takahashi H., Uno T., Tsukamoto T., Hiei K., Fujiwara H., Candesartan decreases carotid intima-media thickness by enhancing nitric oxide and decreasing oxidative stress in patients with hypertension, Hypertension Research, 31, 2, pp. 271-279, (2008)