Ischemia-Reperfusion Injury of the Heart: Moving forward with our Knowledge

Ducas, Annie

doi:10.16966/2379-769x.110

Cited by 3 publications

(1 citation statement)

References 101 publications

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“…However, it is not clear whether the occurrence of cardiac dysfunction is a consequence of events associated with cardiac hypertrophy or is due to some direct action of oxidative stress on cardiomyocytes per se. Further discussion in this report is thus focused to provide evidence that the generation of oxidative stress in non-hypertrophied heart leads to the development of subcellular alterations and cardiac dysfunction [125][126][127][128][129]. Different oxygen reactive species, which result in the development of oxidative stress, have been reported to be involved not only in inducing changes in cardiac contractile activity but are also considered to be mediators of the myocardial cell injury [130][131][132][133][134].…”

Section: Evidence For the Implications Of Oxidative Stress In Cardiac Dysfunction And Subcellular Remodelingmentioning

confidence: 99%

Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure

et al. 2021

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Although heart failure due to a wide variety of pathological stimuli including myocardial infarction, pressure overload and volume overload is associated with cardiac hypertrophy, the exact reasons for the transition of cardiac hypertrophy to heart failure are not well defined. Since circulating levels of several vasoactive hormones including catecholamines, angiotensin II, and endothelins are elevated under pathological conditions, it has been suggested that these vasoactive hormones may be involved in the development of both cardiac hypertrophy and heart failure. At initial stages of pathological stimuli, these hormones induce an increase in ventricular wall tension by acting through their respective receptor-mediated signal transduction systems and result in the development of cardiac hypertrophy. Some oxyradicals formed at initial stages are also involved in the redox-dependent activation of the hypertrophic process but these are rapidly removed by increased content of antioxidants in hypertrophied heart. In fact, cardiac hypertrophy is considered to be an adaptive process as it exhibits either normal or augmented cardiac function for maintaining cardiovascular homeostasis. However, exposure of a hypertrophied heart to elevated levels of circulating hormones due to pathological stimuli over a prolonged period results in cardiac dysfunction and development of heart failure involving a complex set of mechanisms. It has been demonstrated that different cardiovascular abnormalities such as functional hypoxia, metabolic derangements, uncoupling of mitochondrial electron transport, and inflammation produce oxidative stress in the hypertrophied failing hearts. In addition, oxidation of catecholamines by monoamine oxidase as well as NADPH oxidase activation by angiotensin II and endothelin promote the generation of oxidative stress during the prolonged period by these pathological stimuli. It is noteworthy that oxidative stress is known to activate metallomatrix proteases and degrade the extracellular matrix proteins for the induction of cardiac remodeling and heart dysfunction. Furthermore, oxidative stress has been shown to induce subcellular remodeling and Ca2+-handling abnormalities as well as loss of cardiomyocytes due to the development of apoptosis, necrosis, and fibrosis. These observations support the view that a low amount of oxyradical formation for a brief period may activate redox-sensitive mechanisms, which are associated with the development of cardiac hypertrophy. On the other hand, high levels of oxyradicals over a prolonged period may induce oxidative stress and cause Ca2+-handling defects as well as protease activation and thus play a critical role in the development of adverse cardiac remodeling and cardiac dysfunction as well as progression of heart failure.

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