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Targeting Oxidative Stress in Heart Failure

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Systems Biology of Free Radicals and Antioxidants

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Abstract

There has been longstanding recognition that oxidative stress is heightened in the setting of heart failure. Myocardial sources of reactive oxygen species include dysfunctional mitochondria, whereas xanthine oxidase and NADPH oxidases also contribute to myocyte hypertrophy, apoptosis, myocyte slippage, altered calcium handling, and generation of nitrative stress. However, clinical assessment of oxidative stress is challenging due to localization of oxidative processes and analytical challenges. Many standard pharmacologic therapies for heart failure (such as ACE inhibitors or beta-blockers) have anti-oxidative properties, while clinical investigations in drugs targeting specific oxidative stress pathways (e.g., xanthine oxidase inhibitor, coenzyme Q) have been largely inconclusive to date and are still ongoing.

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Acknowledgment

Dr. Tang is supported by National Institutes of Health grants R01HL103931, P20HL113452, P01HL098055, R01HL103866, and the Cleveland Clinic Clinical Research Unit of the Case Western Reserve University CTSA (UL1TR 000439). He has previously received research grant support from Abbott Laboratories, Inc.

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Authors and Affiliations

  1. Case Western Reserve University School of Medicine, Cleveland, OH, USA

    Janet W. Y. Li

  2. Department of Cellular and Molecular Medicine, Cardiovascular Medicine, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Desk J3-4, Cleveland, OH, 44195, USA

    W. H. Wilson Tang

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  1. Janet W. Y. Li
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  2. W. H. Wilson Tang
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Correspondence to W. H. Wilson Tang .

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  1. Department of Pharmacology and Therapeutics, University of British Colombia, Vancouver, British Columbia, Canada

    Ismail Laher

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Li, J.W.Y., Tang, W.H.W. (2014). Targeting Oxidative Stress in Heart Failure. In: Laher, I. (eds) Systems Biology of Free Radicals and Antioxidants. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30018-9_184

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