The DOI matches its Crossref record; 175 of the 175 references it cites were found in a registry or an index.
Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19
Open accessAbstract
Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease. Here, the authors propose that SARS-CoV-2 induces a prothrombotic state, with dysregulated immunothrombosis in lung microvessels and endothelial injury, which drive the clinical manifestations of severe COVID-19. They discuss potential antithrombotic and immunomodulating drugs that are being considered in the treatment of patients with COVID-19.
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Cites
Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China
Huang, C., Wang, Y., Li, X., Ren, L., Zhao, J., Hu, Y., Zhang, L., Fan, G., Xu, J., Gu, X., et al. (2020) · The Lancet · doi:10.1016/s0140-6736(20)30183-5 · Cited by 48,884
COVID-19: consider cytokine storm syndromes and immunosuppression
Mehta, P., McAuley, D. F., Brown, M., Sanchez, E., Tattersall, R. S., & Manson, J. J. (2020) · The Lancet · doi:10.1016/s0140-6736(20)30628-0 · Cited by 9,664
Pathological findings of COVID-19 associated with acute respiratory distress syndrome
Xu, Z., Shi, L., Wang, Y., Zhang, J., Huang, L., Zhang, C., Liu, S., Zhao, P., Liu, H., Zhu, L., et al. (2020) · The Lancet Respiratory Medicine · doi:10.1016/s2213-2600(20)30076-x · Cited by 8,545
Virological assessment of hospitalized patients with COVID-2019
Wölfel, R., Corman, V. M., Guggemos, W., Seilmaier, M., Zange, S., Müller, M. A., Niemeyer, D., Jones, T. C., Vollmar, P., Rothe, C., et al. (2020) · Nature · doi:10.1038/s41586-020-2196-x · Cited by 6,661
Endothelial cell infection and endotheliitis in COVID-19
Varga, Z., Flammer, A. J., Steiger, P., Haberecker, M., Andermatt, R., Zinkernagel, A. S., Mehra, M. R., Schuepbach, R. A., Ruschitzka, F., & Moch, H. (2020) · The Lancet · doi:10.1016/s0140-6736(20)30937-5 · Cited by 6,358
Hamming, I., Timens, W., Bulthuis, M., Lely, A., Navis, G., & van Goor, H. (2004) · The Journal of Pathology · doi:10.1002/path.1570 · Cited by 5,676
Tang, N., Li, D., Wang, X., & Sun, Z. (2020) · Journal of Thrombosis and Haemostasis · doi:10.1111/jth.14768 · Cited by 5,662
Wiersinga, W. J., Rhodes, A., Cheng, A. C., Peacock, S. J., & Prescott, H. C. (2020) · JAMA · doi:10.1001/jama.2020.12839 · Cited by 4,609
The trinity of COVID-19: immunity, inflammation and intervention
Tay, M. Z., Poh, C. M., Rénia, L., MacAry, P. A., & Ng, L. F. P. (2020) · Nature Reviews Immunology · doi:10.1038/s41577-020-0311-8 · Cited by 4,360
Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19
Blanco-Melo, D., Nilsson-Payant, B. E., Liu, W.-C., Uhl, S., Hoagland, D., Møller, R., Jordan, T. X., Oishi, K., Panis, M., Sachs, D., et al. (2020) · Cell · doi:10.1016/j.cell.2020.04.026 · Cited by 4,222
Cited by
The cGAS–STING pathway drives type I IFN immunopathology in COVID-19
Domizio, J. D., Gulen, M. F., Saidoune, F., Thacker, V. V., Yatim, A., Sharma, K., Nass, T., Guenova, E., Schaller, M., Conrad, C., et al. (2022) · Nature · doi:10.1038/s41586-022-04421-w · Cited by 538
Understanding COVID-19-associated coagulopathy
Conway, E. M., Mackman, N., Warren, R. Q., Wolberg, A. S., Mosnier, L. O., Campbell, R. A., Gralinski, L. E., Rondina, M. T., van de Veerdonk, F. L., Hoffmeister, K. M., et al. (2022) · Nature Reviews Immunology · doi:10.1038/s41577-022-00762-9 · Cited by 359
Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation
Mandel, J., Casari, M., Stepanyan, M., Martyanov, A., & Deppermann, C. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23073868 · Cited by 253
Kandhaya‐Pillai, R., Yang, X., Tchkonia, T., Martin, G. M., Kirkland, J. L., & Oshima, J. (2022) · Aging Cell · doi:10.1111/acel.13646 · Cited by 119
“There is pathological evidence that SARS- CoV- 2 infection can be linked to endothelial cell dysfunction, fibrosis, and thrombosis (Bonaventura et al., 2021; Huertas et al., 2020).”
BackgroundThe neurobiology of SARS-CoV-2 infection
Meinhardt, J., Streit, S., Dittmayer, C., Manitius, R. V., Radbruch, H., & Heppner, F. L. (2024) · Nature Reviews Neuroscience · doi:10.1038/s41583-023-00769-8 · Cited by 64
Metadata
- Authors
- Bonaventura, A., Vecchié, A., Dagna, L., Martinod, K., Dixon, D. L., Van Tassell, B. W., Dentali, F., Montecucco, F., Massberg, S., Levi, M., & Abbate, A.
- Venue
- Nature Reviews Immunology
- Published
- 2021-04-06
- Volume
- 21
- Issue
- 5
- Pages
- 319-329
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- OpenAlex
- W3140915421
- Cited by
- 987
- References
- 175
- FWCI
- 25.93
- Type
- journal article
- Language
- en
- Open access
- green
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- Bonaventura, A., Vecchié, A., Dagna, L., Martinod, K., Dixon, D. L., Van Tassell, B. W., Dentali, F., Montecucco, F., Massberg, S., Levi, M., & Abbate, A. (2021). Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19. Nature Reviews Immunology. https://doi.org/10.1038/s41577-021-00536-9
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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.
