Abstract
Under pathophysiological conditions, reactive oxygen species (ROS) levels may increase and cause cell damage and dysfunction targeting primarily the mitochondria. Using an array of scavenging enzymes and antioxidants, the cardiomyocyte and mainly its mitochondria can neutralize ROS. Importantly, besides its damaging effect on cardiomyocytes, ROS play a central role in a number of signal transduction pathways. Whether the effects of this signaling role are beneficial or harmful may depend upon the location, source, and amount of ROS produced, as well as on the overall redox status of the cell. Indeed, accurate delineation of the downstream signaling pathways involved in ROS accumulation is important in order to improve our understanding of these processes and also to facilitate the development of novel therapies. In this chapter, we will discuss how changes in the cellular redox state may affect cardiac pathophysiology, as well as current and developing therapies.
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Marín-García, J. (2013). Heart Mitochondrial ROS and Oxidative Stress. In: Mitochondria and Their Role in Cardiovascular Disease. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-4599-9_10
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DOI: https://doi.org/10.1007/978-1-4614-4599-9_10
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