Abstract
Reactive oxygen species (ROS) are subcellular messengers in signal transductions pathways with both beneficial and deleterious roles. ROS are generated as a by-product of mitochondrial respiration or metabolism or by specific enzymes such as superoxide dismutases, glutathione peroxidase, catalase, peroxiredoxins, and myeloperoxidases. Under physiological conditions, the low levels of ROS production are equivalent to their detoxification, playing a major role in cellular signaling and function. In pathological situations, particularly atherosclerosis or hypertension, the release of ROS exceeds endogenous antioxidant capacity, leading to cell death. At cardiovascular levels, oxidative stress is highly implicated in myocardial infarction, ischemia/reperfusion, or heart failure. Here, we will first detail the physiological role of low ROS production in the heart and the vessels. Indeed, ROS are able to regulate multiple cardiovascular functions, such as cell proliferation, migration, and death. Second, we will investigate the implication of oxidative stress in cardiovascular diseases. Then, we will focus on ROS produced by NAPDH oxidase or during endothelial or mitochondrial dysfunction. Given the importance of oxidative stress at the cardiovascular level, antioxidant therapies could be a real benefit. In the last part of this review, we will detail the new therapeutic strategies potentially involved in cardiovascular protection and currently under study.
Highlights
Cardiovascular diseases are multifactorial disorders that represent the leading causes of death worldwide according to the World Health Organization (WHO) [1]
We will investigate the implication of oxidative stress in cardiovascular diseases and we will focus on reactive oxygen species (ROS) produced by NAPDH oxidase or during endothelial or mitochondrial dysfunction
NADPH oxidases (NOX) activity is increased in patients with a metabolic endothelial, but not cardiac, dysfunction which could be explained by the NOX, constituting the syndrome as well as plasma levels of oxidized low density lipoprotein and nitrotyrosine [32] and a main source of superoxide anion in vessels [30]
Summary
Cardiovascular diseases are multifactorial disorders that represent the leading causes of death worldwide according to the World Health Organization (WHO) [1]. The physiopathology of cardiovascular diseases, mainly caused by atherosclerosis, includes remodeling of blood vessels that can result in blood flow restrictions affecting the heart and the nervous system. The main risk factors for cardiovascular diseases are obesity, diabetes, cigarette smoking, a sedentary and unhealthy lifestyle, and genetic predisposition [1]. Aging is another risk factor, since it increases cardiovascular diseases prevalence mainly due to the accumulation of oxidative damage. Oxidative stress is an important factor involved in cardiovascular diseases progression. We will investigate the implication of oxidative stress in cardiovascular diseases and we will focus on ROS produced by NAPDH oxidase or during endothelial or mitochondrial dysfunction.
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