Abstract
One of the novel interesting topics in the study of cardiovascular disease is the role of the oxidation system, since inflammation and oxidative stress are known to lead to cardiovascular diseases, their progression and complications. During decades of research, many complex interactions between agents of oxidative stress, oxidation, and antioxidant systems have been elucidated, and numerous important pathophysiological links to na number of disorders and diseases have been established. This review article will present the most relevant knowledge linking oxidative stress to vascular dysfunction and disease. The review will focus on the role of oxidative stress in endotheleial dysfunction, atherosclerosis, and other pathogenetic processes and mechanisms that contribute to the development of ischemic heart disease.
Highlights
Atherosclerosis is the most common form of large vessel pathology responsible for syndromes of vital organ ischemic damage like myocardial infarction [1].The key pathophysiologic process of atherosclerosis is chronic inflammation, where oxidative stress plays an essential role in vascular homeostasis regulation including endothelial and smooth muscle cell growth, proliferation, and migration; angiogenesis; apoptosis; vascular tone; host defenses; and genomic stability
Endothelial dysfunction caused by oxidative stress is an early event in the pathogenesis of many cardiovascular diseases including atherosclerosis, dyslipidemia, hypertension, diabetes, chronic kidney disease, heart failure, and ischaemia/ reperfusion injury [18,19,20,21,22,23], and it is a hallmark of vascular diseases
Atherosclerosis is a multisystemic, progressive, chronic inflammatory disease characterized by the interaction of immune and endothelial cells that is mediated by adhesion molecules on the surface of the vascular endothelium leading to the release of numerous proinflammatory mediators [47]
Summary
Atherosclerosis is the most common form of large vessel pathology responsible for syndromes of vital organ ischemic damage like myocardial infarction [1]. The key pathophysiologic process of atherosclerosis is chronic inflammation, where oxidative stress plays an essential role in vascular homeostasis regulation including endothelial and smooth muscle cell growth, proliferation, and migration; angiogenesis; apoptosis; vascular tone; host defenses; and genomic stability. The relation between heart failure and vascular disease is marked by oxidative stress, caused by ischemia, left ventricular (LV) dysfunction, and neuroendocrinological activation. Additional factors like mechanic vascular properties and geometry, hemodynamic forces, and endothelial gene regulation by biomechanical forces (atheroprone and atheroprotective phenotypes), disturbed flow in vascular regions like arches, branches, and bifurcations can promote vascular injury, ROS activity, coronary atherosclerosis, and ischemic heart failure development [6, 7]. The gut microbiota is involved in mediating metabolic processes associated with risk factors for coronary artery disease such as obesity, dyslipidemia, diabetes mellitus, and dyslipidemia. There is a need to elucidate oxidative stress physiology and pathophysiology, to identify novel therapeutic modalities for selective oxidative stress targeting in atherosclerosis [4]
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