ReviewCells2021
Human Vascular Smooth Muscle Function and Oxidative Stress Induced by NADPH Oxidase with the Clinical Implications.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- MicroRNA-155 at the crossroads of inflammation and vascular dysfunction in essential hypertension.Molecular biology reports · 2026Review
- Late-Onset Menopause Attenuates Aortic Stiffness in the Postmenopausal Period.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Article
- Cocoa Shell Extract Restores Redox Balance in Developmental Hypertension in Male Rats: Roles of Nrf2, SOD2 and p-eNOS.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Article
- Harnessing Gasotransmitters to Combat Age-Related Oxidative Stress in Smooth Muscle and Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Oxidative stress in vascular surgical diseases: mechanisms, impacts and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Oxidative and Nitrous Stress Underlies Vascular Malfunction Induced by Ionizing Radiation and Diabetes.Cardiovascular toxicology · 2024Review
- The role of oxidative stress in aortic dissection: a potential therapeutic target.Frontiers in cardiovascular medicine · 2024Review
- Redox Metabolism and Vascular Calcification in Chronic Kidney Disease.Biomolecules · 2023Article
- Endothelial Dysfunction and Chronic Inflammation: The Cornerstones of Vascular Alterations in Age-Related Diseases.International journal of molecular sciences · 2022Review
- Heme Proteins and Kidney Injury: Beyond Rhabdomyolysis.Kidney360 · 2022Review
- NADPH Oxidases in Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction.Antioxidants (Basel, Switzerland) · 2022Review
- Ferroptosis due to Cystathionine γ Lyase/Hydrogen Sulfide Downregulation Under High Hydrostatic Pressure Exacerbates VSMC Dysfunction.Frontiers in cell and developmental biology · 2022Article
- Chemical Constituents, In Vitro Antioxidant Activity and In Silico Study on NADPH Oxidase ofAntioxidants (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.