About: COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response
Creator	Chen, Xiaoyi Jayarangaiah, Apoorva Kumar, Abhishek Jayarangaiah, Amog Kariyanna, Pramod, Theetha
Source	Medline; PMC
abstract	Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and evidence of microthrombi and macrothrombi, both in venous and arterial systems. The underlying mechanisms associated with CAC have been suggested, but not clearly defined. The model of immunothrombosis illustrates the elaborate crosstalk between the innate immune system and coagulation. The rendering of a procoagulant state in COVID-19 involves the interplay of many innate immune pathways. The SARS-CoV2 virus can directly infect immune and endothelial cells, leading to endothelial injury and dysregulation of the immune system. Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. Additional pathways of specific relevance in CAC include cytokine release and complement activation. All these mechanisms have recently been reported in COVID-19. Immunothrombosis provides a comprehensive perspective of the several synergistic pathways pertinent to the pathogenesis of CAC.
has issue date	2020-07-31(xsd:dateTime)
bibo:doi	10.1177/1076029620943293
bibo:pmid	32735131
has license	cc-by-nc
sha1sum (hex)	d26f11fb8d12ea50ae3c222c14ab8fec76059d9c
schema:url	https://doi.org/10.1177/1076029620943293
resource representing a document's title	COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response
has PubMed Central identifier	PMC7401047
has PubMed identifier	32735131
schema:publication	Clin Appl Thromb Hemost
resource representing a document's body	covid:d26f11fb8d12ea50ae3c222c14ab8fec76059d9c#body_text
is schema:about of	named entity 'immune system' named entity 'procoagulant' named entity 'elaborate' named entity 'immune system' named entity 'intravascular' named entity 'order' named entity 'combat' named entity 'Since' named entity 'illness' named entity 'worldwide' named entity 'health care systems' named entity 'innate immune' named entity 'EVIDENCE OF' named entity 'BUT' named entity 'PROFOUND' named entity 'ORDER' named entity 'GLOBAL' named entity 'RELEASE' named entity 'ASSOCIATED' named entity 'THESE' named entity 'CHALLENGES' named entity 'CAC' named entity 'ADDITIONAL' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2' named entity 'NETOSIS' named entity 'EARLY' named entity 'INHIBITION' named entity 'coagulopathy' named entity 'anticoagulant' named entity 'mechanisms' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'virus' named entity 'innate immune system' named entity 'early' named entity 'pandemic' named entity 'suggested' named entity 'rendering' named entity 'innate immune' named entity 'global pandemic' named entity 'COVID-19' named entity 'endothelial' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'tissue factor' named entity 'SARS-CoV2' named entity 'pathogenesis' named entity 'SARS-CoV2' named entity 'Coagulopathy' named entity 'regulatory T cells' named entity 'complement' named entity 'Neutrophil extracellular traps' named entity 'fibrinolytic pathways' named entity 'coagulation' named entity 'endothelial' named entity 'thrombi' named entity 'plasminogen activator inhibitor' named entity 'innate immune' named entity 'capillaries' named entity 'pro-inflammatory' named entity 'tissue factor pathway inhibitor' named entity 'leukocytes' named entity 'thrombotic' named entity 'Factor VIIa' named entity 'vWF' named entity 'purpuric' named entity 'thrombosis' named entity 'glycoprotein' named entity 'endothelial' named entity 'antibody' named entity 'platelets' named entity 'Leukocytes' named entity 'COVID' named entity 'critically ill patients' named entity 'platelets' named entity 'platelet' named entity 'coagulation factors' named entity 'leukocyte'

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