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Review

Human Vascular Smooth Muscle Function and Oxidative Stress Induced by NADPH Oxidase with the Clinical Implications

1
Department of Dental Anesthesiology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto, Tokushima 770-8504, Japan
2
Department of Anesthesiology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto, Tokushima 770-8504, Japan
3
Department of Anesthesiology and Intensive Care, School of Medicine, Hamamatsu University, 1-20-1, Handayama, Hamamatsu City 431-3192, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: Eun Seong Hwang
Cells 2021, 10(8), 1947; https://doi.org/10.3390/cells10081947
Received: 6 July 2021 / Revised: 28 July 2021 / Accepted: 29 July 2021 / Published: 31 July 2021
(This article belongs to the Special Issue Intracellular Regulation Mechanism of Nicotinamide)
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. View Full-Text
Keywords: human vascular smooth muscle; NADPH oxidase; oxidase stress human vascular smooth muscle; NADPH oxidase; oxidase stress
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MDPI and ACS Style

Takaishi, K.; Kinoshita, H.; Kawashima, S.; Kawahito, S. Human Vascular Smooth Muscle Function and Oxidative Stress Induced by NADPH Oxidase with the Clinical Implications. Cells 2021, 10, 1947. https://doi.org/10.3390/cells10081947

AMA Style

Takaishi K, Kinoshita H, Kawashima S, Kawahito S. Human Vascular Smooth Muscle Function and Oxidative Stress Induced by NADPH Oxidase with the Clinical Implications. Cells. 2021; 10(8):1947. https://doi.org/10.3390/cells10081947

Chicago/Turabian Style

Takaishi, Kazumi, Hiroyuki Kinoshita, Shingo Kawashima, and Shinji Kawahito. 2021. "Human Vascular Smooth Muscle Function and Oxidative Stress Induced by NADPH Oxidase with the Clinical Implications" Cells 10, no. 8: 1947. https://doi.org/10.3390/cells10081947

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