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dc.contributor.authorWang, Xin
dc.contributor.authorSahu, Kamal Kant
dc.contributor.authorCerny, Jan
dc.date2022-08-11T08:08:09.000
dc.date.accessioned2022-08-23T15:44:36Z
dc.date.available2022-08-23T15:44:36Z
dc.date.issued2020-10-15
dc.date.submitted2020-10-26
dc.identifier.citation<p>Wang X, Sahu KK, Cerny J. Coagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complement system inhibition in COVID-19. J Thromb Thrombolysis. 2020 Oct 15:1–6. doi: 10.1007/s11239-020-02297-z. Epub ahead of print. PMID: 33063256; PMCID: PMC7561230. <a href="https://doi.org/10.1007/s11239-020-02297-z">Link to article on publisher's site</a></p>
dc.identifier.issn0929-5305 (Linking)
dc.identifier.doi10.1007/s11239-020-02297-z
dc.identifier.pmid33063256
dc.identifier.urihttp://hdl.handle.net/20.500.14038/27349
dc.description.abstractCoronavirus disease-2019 (COVID-19) is a rapidly evolving health crisis caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a novel disease entity and we are in a learning phase with regards to the pathogenesis, disease manifestations, and therapeutics. In addition to the primary lung injury, many patients especially the ones with moderate to severe COVID-19 display evidence of endothelial damage, complement activation, which leads to a pro-coagulable state. While there are still missing links in our understanding, the interplay of endothelium, complement system activation, and immune response to the SARS-CoV-2 virus is a surprisingly major factor in COVID-19 pathogenesis. One could envision COVID-19 becoming a novel hematological syndrome. This review is to discuss the available literature with regards to the involvement of the complement system, and coagulation cascade and their interaction with endothelium.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=33063256&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561230/
dc.subjectCOVID-19
dc.subjectCoronavirus
dc.subjectImmunity
dc.subjectPandemic
dc.subjectCardiovascular Diseases
dc.subjectFluids and Secretions
dc.subjectHematology
dc.subjectHemic and Immune Systems
dc.subjectHemic and Lymphatic Diseases
dc.subjectImmunity
dc.subjectInfectious Disease
dc.subjectRespiratory Tract Diseases
dc.subjectVirus Diseases
dc.titleCoagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complement system inhibition in COVID-19
dc.typeJournal Article
dc.source.journaltitleJournal of thrombosis and thrombolysis
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/covid19/140
dc.identifier.contextkey19982556
html.description.abstract<p>Coronavirus disease-2019 (COVID-19) is a rapidly evolving health crisis caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a novel disease entity and we are in a learning phase with regards to the pathogenesis, disease manifestations, and therapeutics. In addition to the primary lung injury, many patients especially the ones with moderate to severe COVID-19 display evidence of endothelial damage, complement activation, which leads to a pro-coagulable state. While there are still missing links in our understanding, the interplay of endothelium, complement system activation, and immune response to the SARS-CoV-2 virus is a surprisingly major factor in COVID-19 pathogenesis. One could envision COVID-19 becoming a novel hematological syndrome. This review is to discuss the available literature with regards to the involvement of the complement system, and coagulation cascade and their interaction with endothelium.</p>
dc.identifier.submissionpathcovid19/140
dc.contributor.departmentDepartment of Medicine, Hematology and Oncology


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