The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
COVID-19 is, in the end, an endothelial disease
Open accessAbstract
The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.
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Citations
Cites
Dexamethasone in Hospitalized Patients with Covid-19
The RECOVERY Collaborative Group (2021) · New England Journal of Medicine · doi:10.1056/nejmoa2021436 · Cited by 11,477
Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19
Ackermann, M., Verleden, S. E., Kuehnel, M., Haverich, A., Welte, T., Laenger, F., Vanstapel, A., Werlein, C., Stark, H., Tzankov, A., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa2015432 · Cited by 5,613
Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis
Gimbrone, M. A., & García-Cardeña, G. (2016) · Circulation Research · doi:10.1161/circresaha.115.306301 · Cited by 3,476
Effective treatment of severe COVID-19 patients with tocilizumab
Xu, X., Han, M., Li, T., Sun, W., Wang, D., Fu, B., Zhou, Y., Zheng, X., Yang, Y., Li, X., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2005615117 · Cited by 2,647
Autopsy Findings and Venous Thromboembolism in Patients With COVID-19: A Prospective Cohort Study
Wichmann, D., Sperhake, J.-P., Lütgehetmann, M., Steurer, S., Edler, C., Heinemann, A., Heinrich, F., Mushumba, H., Kniep, I., Schröder, A. S., et al. (2020) · Annals of Internal Medicine · doi:10.7326/m20-2003 · Cited by 2,274
Evolving functions of endothelial cells in inflammation
Pober, J. S., & Sessa, W. C. (2007) · Nature Reviews Immunology · doi:10.1038/nri2171 · Cited by 2,022
Neutrophil extracellular traps in COVID-19
Zuo, Y., Yalavarthi, S., Shi, H., Gockman, K., Zuo, M., Madison, J. A., Blair, C. N., Weber, A., Barnes, B. J., Egeblad, M., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.138999 · Cited by 1,582
Targeting potential drivers of COVID-19: Neutrophil extracellular traps
Barnes, B. J., Adrover, J. M., Baxter-Stoltzfus, A., Borczuk, A., Cools-Lartigue, J., Crawford, J. M., Daßler-Plenker, J., Guerci, P., Huynh, C., Knight, J. S., et al. (2020) · Journal of Experimental Medicine · doi:10.1084/jem.20200652 · Cited by 1,486
Cavalli, G., De Luca, G., Campochiaro, C., Della-Torre, E., Ripa, M., Canetti, D., Oltolini, C., Castiglioni, B., Tassan Din, C., Boffini, N., et al. (2020) · The Lancet Rheumatology · doi:10.1016/s2665-9913(20)30127-2 · Cited by 970
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Self-citation
Cited by
Nalbandian, A., Sehgal, K., Gupta, A., Madhavan, M. V., McGroder, C., Stevens, J. S., Cook, J. R., Nordvig, A. S., Shalev, D., Sehrawat, T. S., et al. (2021) · Nature Medicine · doi:10.1038/s41591-021-01283-z · Cited by 4,862
Fatigue and cognitive impairment in Post-COVID-19 Syndrome: a systematic review and meta-analysis
Ceban, F., Ling, S., Lui, L. M. W., Lee, Y., Gill, H., Teopiz, K. M., Rodrigues, N. B., Subramaniapillai, M., Di Vincenzo, J. D., Cao, B., et al. (2022) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2021.12.020 · Cited by 1,554
Targeting inflammation in atherosclerosis — from experimental insights to the clinic
Soehnlein, O., & Libby, P. (2021) · Nature Reviews Drug Discovery · doi:10.1038/s41573-021-00198-1 · Cited by 1,019
Self-citationLong COVID: post-acute sequelae of COVID-19 with a cardiovascular focus
Raman, B., Bluemke, D. A., Lüscher, T. F., & Neubauer, S. (2022) · European Heart Journal · doi:10.1093/eurheartj/ehac031 · Cited by 650
Self-citationKomaroff, A. L., & Lipkin, W. I. (2021) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2021.06.002 · Cited by 259
Metadata
- Authors
- Libby, P., & Lüscher, T.
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-08-21
- Volume
- 41
- Issue
- 32
- Pages
- 3038-3044
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- OpenAlex
- W3082240102
- Cited by
- 961
- References
- 61
- FWCI
- 22.60
- Type
- journal article
- Language
- en
- Open access
- bronze
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