Abstract
Reactive oxygen species (ROS) are highly reactive chemical species containing oxygen, controlled by both enzymatic and nonenzymatic antioxidant defense systems. In the heart, ROS play an important role in cell homeostasis, by modulating cell proliferation, differentiation, and excitation-contraction coupling. Oxidative stress occurs when ROS production exceeds the buffering capacity of the antioxidant defense systems, leading to cellular and molecular abnormalities, ultimately resulting in cardiac dysfunction. In this review, we will discuss the physiological sources of ROS in the heart, the mechanisms of oxidative stress-related myocardial injury, and the implications of experimental studies and clinical trials with antioxidant therapies in cardiovascular diseases.
Highlights
Reactive oxygen species (ROS) are highly reactive chemical species containing oxygen, including the superoxide (O2-) and the hydroxyl (OH-) anions, and hydrogen peroxide (H2O2)
Supplements for the primary or secondary prevention of major cardiovascular events [330]. These supplements are not associated with any reduced risk of such events in the subgroup meta-analyses according to various factors, including type of vitamins and antioxidants, type of cardiovascular outcomes, study design, methodological quality, duration of treatment, funding source, provider of supplements, type of control, number of participants in each trial, and supplements given singly or in combination with other vitamins or antioxidant supplements [330]. These findings suggest that most antioxidative stress therapies have failed in providing solid evidence of clinical benefits, even though the exact reasons and mechanisms remain unknown
ROS represent important second messengers within the heart, since they are involved in multiple physiological processes including differentiation, proliferation, and excitation-contraction coupling (Figure 2)
Summary
Reactive oxygen species (ROS) are highly reactive chemical species containing oxygen, including the superoxide (O2-) and the hydroxyl (OH-) anions, and hydrogen peroxide (H2O2). Minhas et al have supported the idea that XOR is the primary source of ROS generation in the failing heart and that its upregulation contributes to maladaptive cardiac hypertrophy, directly participating in the progression of LV failure, since chronic XO inhibition with oxypurinol reverses left ventricular (LV) remodeling and improves LV function following experimental myocardial infarction in rats [38]. The NADPH oxidases (Nox) are a family of seven membrane-bound enzymes and represent the major sources of ROS in the cardiovascular system [52,53,54] They catalyze the reduction of molecular oxygen to O2by using NADPH as electron donor. Genetic deletion of MAO-B protects against oxidative stress, apoptosis, and ventricular dysfunction in a model of pressure overload [85]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
