The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Dysfunction of Endothelial Nitric Oxide Synthase and Atherosclerosis
Abstract
Atherosclerosis is associated with an impairment of endothelium-dependent relaxations, which represents the reduced bioavailability of nitric oxide (NO) produced from endothelial NO synthase (eNOS). Among various mechanisms implicated in the impaired EDR in atherosclerosis, superoxide generated from dysfunctional eNOS has attracted attention. Under conditions in which vascular tissue levels of tetrahydrobiopterin (BH4), a cofactor for NOS, are deficient or lacking, eNOS becomes dysfunctional and produces superoxide rather than NO. Experimental studies in vitro have revealed that NO from eNOS constitutes an anti-atherogenic molecule. A deficiency of eNOS was demonstrated to accelerate atherosclerotic lesion formation in eNOS knockout mice. In contrast, eNOS overexpression with hypercholesterolemia may promote atherogenesis via increased superoxide generation from dysfunctional eNOS. Thus, eNOS may have 2 faces in the pathophysiology of atherosclerosis depending on tissue BH4 metabolisms. An improved understanding of tissue BH4 metabolisms in atherosclerotic vessels is needed, which would help in developing new strategies for the inhibition and treatment of atherosclerosis.
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Cites
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Cited by
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363
Balligand, J.-L., Feron, O., & Dessy, C. (2009) · Physiological Reviews · doi:10.1152/physrev.00042.2007 · Cited by 477
Ouchi, N., Oshima, Y., Ohashi, K., Higuchi, A., Ikegami, C., Izumiya, Y., & Walsh, K. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m803440200 · Cited by 338
Wang, Y., Zhao, X., Jin, H., Wei, H., Li, W., Bu, D., Tang, X., Ren, Y., Tang, C., & Du, J. (2009) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.108.179333 · Cited by 307
Body temperature regulation in diabetes
Kenny, G. P., Sigal, R. J., & McGinn, R. (2016) · Temperature · doi:10.1080/23328940.2015.1131506 · Cited by 297
“adversely alter endothelial function through interfering with nitric oxide signaling.(110) In fact, one study reported that the relative nitric oxide-dependent vasodilation during whole-body passive heating was similar between healthy controls and those with type 2 diabetes; however, absolute skin blood flow was lower…”
Background
Metadata
- Authors
- Kawashima, S., & Yokoyama, M.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2004-06
- Volume
- 24
- Issue
- 6
- Pages
- 998-1005
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W1992547254
- Cited by
- 453
- References
- 14
- FWCI
- 14.06
- Type
- journal article
- Language
- en
- Open access
- closed
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- Kawashima, S., & Yokoyama, M. (2004). Dysfunction of Endothelial Nitric Oxide Synthase and Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/01.atv.0000125114.88079.96
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
