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Reactive Oxygen Species (ROS) and Cardiac Ischemia and Reperfusion Injury

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Abstract

A growing body of evidence suggests that oxidative stress and nitrosative stress are the common denominators in many disorders, including cardiac ischemia and reperfusion (I/R) injury resulting from coronary vascular disease. In acute myocardial infarction, two distinct types of damage occur to the heart: ischemic injury and reperfusion injury. Both ischemia and reperfusion are individually important in the manifestation of I/R injury. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are well recognized for playing dual roles as both beneficial and harmful reactive species. ROS generation from myriad sources may contribute to tissue infarction, but mitochondrial sources of ROS, particularly from cardiomyocytes, are considered the primary sites for ROS generation during I/R. During myocardial oxidative stress (excess ROS) the generation of ROS is enhanced and the antioxidant defense mechanisms are compromised. Excess ROS can cause a feed-forward effect on further ROS generation (ROS-induced-ROS release), which is also linked to mitochondrial Ca2+ overload. These factors lead to mitochondrial dysfunction manifested as mitochondrial permeability transition pore opening and mitochondrial outer membrane permeabilization with concomitant release of apoptotic factors, inhibition of oxidative phosphorylation, depletion of cellular ATP, and subsequent cell death by apoptosis and/or necrosis. This book chapter will present a broad overview on the most current state in the discussion of the role of ROS/RNS and redox signaling in cardiac I/R injury and on potential therapeutic approaches to mitigate infarction and no-reflow following an ischemic episode.

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Acknowledgments

The authors wish to thank Mohammed Aldakkak MD and Christoph Blomeyer MD for reading and critiquing the manuscript. The writing of this chapter was supported in part by grants from the National Institutes of Health (HL095122-Camara AKS/Dash RK; HL089514, HL098490-Stowe DF; P01GM066730-Bosnjak ZB; and the Veterans Administration (Merit Review 8204-05P-Stowe DF).

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Correspondence to Amadou K. S. Camara .

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Camara, A.K.S., Stowe, D.F. (2014). Reactive Oxygen Species (ROS) and Cardiac Ischemia and Reperfusion Injury. In: Laher, I. (eds) Systems Biology of Free Radicals and Antioxidants. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30018-9_75

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