The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Vascular endothelial dysfunction and pharmacological treatment
Open accessAbstract
The endothelium exerts multiple actions involving regulation of vascular permeability and tone, coagulation and fibrinolysis, inflammatory and immunological reactions and cell growth. Alterations of one or more such actions may cause vascular endothelial dysfunction. Different risk factors such as hypercholesterolemia, homocystinemia, hyperglycemia, hypertension, smoking, inflammation, and aging contribute to the development of endothelial dysfunction. Mechanisms underlying endothelial dysfunction are multiple, including impaired endothelium-derived vasodilators, enhanced endothelium-derived vasoconstrictors, over production of reactive oxygen species and reactive nitrogen species, activation of inflammatory and immune reactions, and imbalance of coagulation and fibrinolysis. Endothelial dysfunction occurs in many cardiovascular diseases, which involves different mechanisms, depending on specific risk factors affecting the disease. Among these mechanisms, a reduction in nitric oxide (NO) bioavailability plays a central role in the development of endothelial dysfunction because NO exerts diverse physiological actions, including vasodilation, anti-inflammation, antiplatelet, antiproliferation and antimigration. Experimental and clinical studies have demonstrated that a variety of currently used or investigational drugs, such as angiotensin-converting enzyme inhibitors, angiotensin AT1 receptors blockers, angiotensin-(1-7), antioxidants, beta-blockers, calcium channel blockers, endothelial NO synthase enhancers, phosphodiesterase 5 inhibitors, sphingosine-1-phosphate and statins, exert endothelial protective effects. Due to the difference in mechanisms of action, these drugs need to be used according to specific mechanisms underlying endothelial dysfunction of the disease.
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Cites
Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation
Dimmeler, S., Fleming, I., Fisslthaler, B., Hermann, C., Busse, R., & Zeiher, A. M. (1999) · Nature · doi:10.1038/21224 · Cited by 3,591
Landmesser, U., Dikalov, S., Price, S. R., McCann, L., Fukai, T., Holland, S. M., Mitch, W. E., & Harrison, D. G. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200314172 · Cited by 1,660
Fox, K., Ford, I., Steg, P. G., Tendera, M., & Ferrari, R. (2008) · The Lancet · doi:10.1016/s0140-6736(08)61170-8 · Cited by 1,099
S-glutathionylation uncouples eNOS and regulates its cellular and vascular function
Chen, C.-A., Wang, T.-Y., Varadharaj, S., Reyes, L. A., Hemann, C., Talukder, M. A. H., Chen, Y.-R., Druhan, L. J., & Zweier, J. L. (2010) · Nature · doi:10.1038/nature09599 · Cited by 594
Antioxidant Vitamin C Improves Endothelial Dysfunction in Chronic Smokers
Heitzer, T., Just, H., & Mu¨nzel, T. (1996) · Circulation · doi:10.1161/01.cir.94.1.6 · Cited by 554
NADH oxidoreductase is a major source of superoxide anion in bovine coronary artery endothelium
Mohazzab, K. M., Kaminski, P. M., & Wolin, M. S. (1994) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1994.266.6.h2568 · Cited by 536
Duplain, H., Burcelin, R., Sartori, C., Cook, S., Egli, M., Lepori, M., Vollenweider, P., Pedrazzini, T., Nicod, P., Thorens, B., et al. (2001) · Circulation · doi:10.1161/01.cir.104.3.342 · Cited by 533
Antoniades, C., Bakogiannis, C., Leeson, P., Guzik, T. J., Zhang, M.-H., Tousoulis, D., Antonopoulos, A. S., Demosthenous, M., Marinou, K., Hale, A., et al. (2011) · Circulation · doi:10.1161/circulationaha.110.985150 · Cited by 219
TANG, Z., JIANG, L., PENG, J., REN, Z., WEI, D., WU, C., PAN, L., JIANG, Z., & LIU, L. (2012) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2012.1072 · Cited by 208
PCSK9 siRNA inhibits HUVEC apoptosis induced by ox-LDL via Bcl/Bax-caspase9-caspase3 pathway
Wu, C.-Y., Tang, Z.-H., Jiang, L., Li, X.-F., Jiang, Z.-S., & Liu, L.-S. (2012) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-011-1028-6 · Cited by 190
Cited by
Endothelial Dysfunction and Hypertension
Konukoglu, D., & Uzun, H. (2016) · Advances in Experimental Medicine and Biology · doi:10.1007/5584_2016_90 · Cited by 594
Epidemiology and Immune Pathogenesis of Viral Sepsis
Lin, G.-L., McGinley, J. P., Drysdale, S. B., & Pollard, A. J. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.02147 · Cited by 351
Mechanisms of long COVID and the path toward therapeutics
Peluso, M. J., & Deeks, S. G. (2024) · Cell · doi:10.1016/j.cell.2024.07.054 · Cited by 341
The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art
Esse, R., Barroso, M., Tavares de Almeida, I., & Castro, R. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040867 · Cited by 336
Scioli, M. G., Storti, G., D’Amico, F., Rodríguez Guzmán, R., Centofanti, F., Doldo, E., Céspedes Miranda, E. M., & Orlandi, A. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9061995 · Cited by 281
Metadata
- Authors
- Su, J. B.
- Venue
- World Journal of Cardiology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2015
- Volume
- 7
- Issue
- 11
- Pages
- 719
- ISSN
- 1949-8462 (ISSN-L)
- OpenAlex
- W2193994735
- Cited by
- 238
- References
- 11
- FWCI
- 12.91
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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