The DOI matches its Crossref record; 84 of the 84 references it cites were found in a registry or an index.
The vascular NAD(P)H oxidases as therapeutic targets in cardiovascular diseases
Abstract
Activation of vascular NAD(P)H oxidases and the production of reactive oxygen species (ROS) by these enzyme systems are common in cardiovascular disease. In the past several years, a new family of NAD(P)H oxidase subunits, known as the non-phagocytic NAD(P)H oxidase (NOX) proteins, have been discovered and shown to play a role in vascular tissues. Recent studies make clearer the mechanisms of activation of the endothelial and vascular smooth muscle NAD(P)H oxidases. ROS produced following angiotensin II-mediated stimulation of NAD(P)H oxidases signal through pathways such as mitogen-activated protein kinases, tyrosine kinases and transcription factors, and lead to events such as inflammation, hypertrophy, remodeling and angiogenesis. Studies in mice that are deficient in p47(phox) and gp91(phox) (also known as NOX2) NAD(P)H oxidase subunits show that ROS produced by these oxidases contribute to cardiovascular diseases including atherosclerosis and hypertension. Recently, efforts have been devoted to developing inhibitors of NAD(P)H oxidases that will provide useful experimental tools and might have therapeutic potential in the treatment of human diseases.
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“The current knowledge about NOX enzymes in the cardiovascular system indicates that NOX2 is usually the main player in the development of pathological conditions and increased NOX2 activity is linked to vascular disease (142, 252, 478).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [142]
In the citing paper
“The current knowledge about NOX enzymes in the cardiovascular system indicates that NOX2 is usually the main player in the development of pathological conditions and increased NOX2 activity is linked to vascular disease (142, 252, 478).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [142]
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2 retracted
Ushio‐Fukai, M., Tang, Y., Fukai, T., Dikalov, S., Ma, Y., Fujimoto, M., Quinn, M. T., Pagano, P. J., Johnson, C., & Alexander, R. W. (2002) · Circulation Research · doi:10.1161/01.res.0000046227.65158.f8 · Cited by 466
RetractedUshio‐Fukai, M., Griendling, K. K., Becker, P. L., Hilenski, L. L., Halleran, S., & Alexander, R. W. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.21.4.489 · Cited by 283
Self-citationRetractedEndothelial dysfunction in cardiovascular diseases: the role of oxidant stress
Cai, H., & Harrison, D. G. (2000) · Circulation Research · doi:10.1161/01.res.87.10.840 · Cited by 3,839
Self-citationNAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
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Self-citationAngiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.
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Self-citationMatrix Metalloproteinases in Vascular Remodeling and Atherogenesis
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Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly.
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Self-citationLandmesser, U., Dikalov, S., Price, S. R., McCann, L. A., Fukai, T., Holland, S. M., Mitch, W. E., & Harrison, D. G. (2003) · Journal of Clinical Investigation · doi:10.1172/jci14172 · Cited by 1,652
Self-citation
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Cited by
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Neurovascular regulation in the normal brain and in Alzheimer's disease
Iadecola, C. (2004) · Nature Reviews Neuroscience · doi:10.1038/nrn1387 · Cited by 2,213
Physiology of Local Renin-Angiotensin Systems
Paul, M., Poyan Mehr, A., & Kreutz, R. (2006) · Physiological Reviews · doi:10.1152/physrev.00036.2005 · Cited by 1,739
Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
Guzik, T. J., Hoch, N. E., Brown, K. A., McCann, L. A., Rahman, A., Dikalov, S., Goronzy, J., Weyand, C., & Harrison, D. G. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070657 · Cited by 1,736
Self-citationNeurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease
Girouard, H., & Iadecola, C. (2005) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00966.2005 · Cited by 1,311
Reactive Oxygen Species, Vascular Oxidative Stress, and Redox Signaling in Hypertension
Touyz, R. M. (2004) · Hypertension · doi:10.1161/01.hyp.0000138070.47616.9d · Cited by 870
Metadata
- Authors
- Cai, H., Griendling, K. K., & Harrison, D. G.
- Affiliations
- Emory University (US)
- Corresponding author
- Harrison, David G
- Venue
- Trends in Pharmacological Sciences
- Publisher
- Elsevier BV
- Published
- 2003-09
- Volume
- 24
- Issue
- 9
- Pages
- 471-478
- ISSN
- 0165-6147 (ISSN-L)
- OpenAlex
- W2000155150
- Cited by
- 687
- References
- 84
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 13 · 2023: 3 · 2022: 9 · 2021: 12 · 2020: 18 · 2019: 11 · 2018: 13 · 2017: 10 · 2016: 26 · 2015: 25 · 2014: 32 · 2013: 35 · 2012: 47
- FWCI
- 8.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Pharmacological Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- NADPH oxidase, reactive oxygen species, cardiovascular disease, p47phox, gp91phox, NOX2, angiotensin II, vascular smooth muscle, atherosclerosis, hypertension, therapeutic target, inflammation, vascular remodeling, angiogenesis
- MeSH terms
- Angiotensin II, Animals, Blood Vessels, Cardiovascular Agents, Cardiovascular Diseases, Enzyme Activation, Humans, Reactive Oxygen Species, NADPH Oxidases, Mice
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