Abstract
The “Oxygen Paradox” proposes that it is tough for aerobic organisms to live without oxygen, but it is difficult to live with oxygen as well. Assigned a job of incessant pumping, the heart, being an obligate aerobic organ, epitomizes the paradoxical effects of oxygen. Much of them are attributed to the reactive oxygen species (ROS) that mold the embryonic development and normal functioning of the heart under homeostatic conditions on one hand and the progression of cardiovascular diseases on the other. The ROS generation within the heart is equated at controlled physiological levels to the scavenger endogenous antioxidants that are employed to prevent their accumulation. A shift in the balance causes toxic levels of ROS to accumulate, self-accentuate, and inflict damage to cellular components, leading to myocardial oxidative injury. In addition, a number of pathophysiological signalling pathways are triggered by amassed ROS which culminate into enhanced myocardial apoptosis, fibrosis, inflammation, and contractile dysfunction—hallmarks of a failing heart. Adverse left ventricular remodeling as in pathological cardiac hypertrophy and myocardial infarction is intricately associated with oxidative stress, which prompts researchers to focus their attention on the redox biology of the heart in health and disease. This has been yielding far-reaching clinical implications in the field of antioxidant therapy and redox biomarker discovery. As cardiac disorders continue to be the highest contributor to the Global Burden of Disease, a molecular detailing of where, what, when, and how ROS is conducive to the remodeling of the cellular milieu in the heart would provide a holistic appreciation of cardiac disease biology.
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Chaudhuri, R.D., Rana, S., Datta, K., Sarkar, S. (2019). Key Cellular Effectors in ROS-Mediated Cardiac Diseases. In: Chakraborti, S., Dhalla, N., Dikshit, M., Ganguly, N. (eds) Modulation of Oxidative Stress in Heart Disease. Springer, Singapore. https://doi.org/10.1007/978-981-13-8946-7_7
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