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Oxidative Stress and Heart Failure

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Heart Failure

Part of the book series: Contemporary Cardiology ((CONCARD))

Abstract

Heart failure (HF) is a complex clinical syndrome whose pathogenesis includes an interplay of neurohormonal and inflammatory processes at the cellular and molecular levels. Oxidative stress (OS) may represent the common pathway for cell death/apoptosis, cardiac remodeling, and dysfunction. There is increasing evidence to indicate that reactive oxygen species (ROS) plays an important role in the development and progression of HF. However, while levels of ROS are elevated in HF, the relative contribution of the different intracellular sources of ROS and the precise mechanisms of this increase remains unclear. Further delineation of the downstream signaling pathways involved in ROS accumulation is important, in order to improve our understanding of these processes and also for the development of new therapies. Indeed, despite previously disappointing results from using antioxidants in human studies, it is likely that modulation of endogenous antioxidants in human HF will continue to have the potential for both, treatment and prevention. In this chapter, we will look at how changes in the cellular redox state of cardiovascular tissue affect the development and progression of HF. In addition, the potential sources of ROS involved in the HF syndrome will be discussed.

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Marín-García, J. (2010). Oxidative Stress and Heart Failure. In: Heart Failure. Contemporary Cardiology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-147-9_10

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