The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Tissue Angiotensin and Pathobiology of Vascular Disease: A Unifying Hypothesis
Open accessAbstract
Abstract —There is increasing evidence that direct pathobiological events in the vessel wall play an important role in vascular disease. An important mechanism involves the perturbation of the homeostatic balance between NO and reactive oxygen species. Increased reactive oxygen species can inactivate NO and produce peroxynitrite. Angiotensin II is a potent mediator of oxidative stress and stimulates the release of cytokines and the expression of leukocyte adhesion molecules that mediate vessel wall inflammation. Inflammatory cells release enzymes (including ACE) that generate angiotensin II. Thus, a local positive-feedback mechanism could be established in the vessel wall for oxidative stress, inflammation, and endothelial dysfunction. Angiotensin II also acts as a direct growth factor for vascular smooth muscle cells and can stimulate the local production of metalloproteinases and plasminogen activator inhibitor. Taken together, angiotensin II can promote vasoconstriction, inflammation, thrombosis, and vascular remodeling. In this article, we propose a model that unifies the interrelationship among cardiovascular risk factors, angiotensin II, and the pathobiological mechanisms contributing to cardiovascular disease. This model may also explain the beneficial effects of ACE inhibitors on cardiovascular events beyond blood pressure reduction.
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Cited by
Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases
Phaniendra, A., Jestadi, D. B., & Periyasamy, L. (2015) · Indian Journal of Clinical Biochemistry · doi:10.1007/s12291-014-0446-0 · Cited by 2,886
Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system
Mehta, P. K., & Griendling, K. K. (2007) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00287.2006 · Cited by 1,924
Mazzali, M., Kanellis, J., Han, L., Feng, L., Xia, Y.-Y., Chen, Q., Kang, D.-H., Gordon, K. L., Watanabe, S., Nakagawa, T., et al. (2002) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00283.2001 · Cited by 826
Endothelial Function and Oxidative Stress in Cardiovascular Diseases
Higashi, Y., Noma, K., Yoshizumi, M., & Kihara, Y. (2009) · Circulation Journal · doi:10.1253/circj.cj-08-1102 · Cited by 798
Rosendorff, C., Black, H. R., Cannon, C. P., Gersh, B. J., Gore, J., Izzo, J. L., Kaplan, N. M., O’Connor, C. M., O’Gara, P. T., & Oparil, S. (2007) · Circulation · doi:10.1161/circulationaha.107.183885 · Cited by 757
Metadata
- Authors
- Dzau, V. J.
- Venue
- Hypertension
- Published
- 2001-04
- Volume
- 37
- Issue
- 4
- Pages
- 1047-1052
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2119869567
- Cited by
- 750
- References
- 6
- FWCI
- 36.96
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
