Abstract
Among reactive oxygen species, superoxide mediates the critical vascular redox signaling, resulting in the regulation of the human cardiovascular system. The reduced form of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase, NOX) is the source of superoxide and relates to the crucial intracellular pathology and physiology of vascular smooth muscle cells, including contraction, proliferation, apoptosis, and inflammatory response. Human vascular smooth muscle cells express NOX1, 2, 4, and 5 in physiological and pathological conditions, and those enzymes play roles in most cardiovascular disorders caused by hypertension, diabetes, inflammation, and arteriosclerosis. Various physiologically active substances, including angiotensin II, stimulate NOX via the cytosolic subunits’ translocation toward the vascular smooth muscle cell membrane. As we have shown, some pathological stimuli such as high glucose augment the enzymatic activity mediated by the phosphatidylinositol 3-kinase-Akt pathway, resulting in the membrane translocation of cytosolic subunits of NOXs. This review highlights and details the roles of human vascular smooth muscle NOXs in the pathophysiology and clinical aspects. The regulation of the enzyme expressed in the vascular smooth muscle cells may lead to the prevention and treatment of human cardiovascular diseases.
Highlights
Published: 31 July 2021Increased intracellular calcium, inducing actin-myosin cross-bridge formation, causes vascular smooth muscle contraction [1,2]
We summarize findings, including the critical role of superoxide in vascular oxidative stress, expressed variable NOXs, pathophysiology related to oxidative stress induced by NOXs, and the relationship between vascular pathophysiology induced by NOXs and pharmaceutical formulation in the perioperative period regarding the human vascular smooth muscle cells
Serum derived from patients with chronic kidney disease induces NOX1 upregulation with an elevation of reactive oxygen species and calcium deposition in primary vascular smooth muscle cells [43]
Summary
Increased intracellular calcium, inducing actin-myosin cross-bridge formation, causes vascular smooth muscle contraction [1,2]. The vascular smooth muscle cell function plays a significant role in developing various cardiovascular diseases. The condition enhances diverse intracellular redox signaling pathways following the induction of many cardiovascular pathologies, including arteriosclerosis in human vascular smooth muscle cells, Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. This article focuses on superoxide’s critical roles and each NOX contributing to oxidative stress in human vascular smooth muscle cells. We summarize findings, including the critical role of superoxide in vascular oxidative stress, expressed variable NOXs, pathophysiology related to oxidative stress induced by NOXs, and the relationship between vascular pathophysiology induced by NOXs and pharmaceutical formulation in the perioperative period regarding the human vascular smooth muscle cells
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