About: Pulmonary Artery Thrombosis: A Diagnosis That Strives for Its Independence

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Pulmonary Artery Thrombosis: A Diagnosis That Strives for Its Independence
Creator	Lobastov, Kirill Brill, Alexander Brill@bham, A Kravchuk, Viacheslav Laberko, Leonid Porembskaya, Olga Ru, Olga Saiganov, Sergey Tomson, Vladimir Toropova, Yana Uk, A
Source	PMC
abstract	According to a widespread theory, thrombotic masses are not formed in the pulmonary artery (PA) but result from migration of blood clots from the venous system. This concept has prevailed in clinical practice for more than a century. However, a new technologic era has brought forth more diagnostic possibilities, and it has been shown that thrombotic masses in the PA could, in many cases, be found without any obvious source of emboli. Chronic obstructive pulmonary disease, asthma, sickle cell anemia, emergency and elective surgery, viral pneumonia, and other conditions could be complicated by PA thrombosis development without concomitant deep vein thrombosis (DVT). Different pathologies have different causes for local PA thrombotic process. As evidenced by experimental results and clinical observations, endothelial and platelet activation are the crucial mechanisms of this process. Endothelial dysfunction can impair antithrombotic function of the arterial wall through downregulation of endothelial nitric oxide synthase (eNOS) or via stimulation of adhesion receptor expression. Hypoxia, proinflammatory cytokines, or genetic mutations may underlie the procoagulant phenotype of the PA endothelium. Both endotheliocytes and platelets could be activated by protease mediated receptor (PAR)- and receptors for advanced glycation end (RAGE)-dependent mechanisms. Hypoxia, in particular induced by high altitudes, could play a role in thrombotic complications as a trigger of platelet activity. In this review, we discuss potential mechanisms of PA thrombosis in situ.
has issue date	2020-07-18(xsd:dateTime)
bibo:doi	10.3390/ijms21145086
bibo:pmid	32708482
has license	cc-by
sha1sum (hex)	37fc8c0f7e984ab7aaa63b3ddc592717116bfe2f
schema:url	https://doi.org/10.3390/ijms21145086
resource representing a document's title	Pulmonary Artery Thrombosis: A Diagnosis That Strives for Its Independence
has PubMed Central identifier	PMC7404175
has PubMed identifier	32708482
schema:publication	Int J Mol Sci
resource representing a document's body	covid:37fc8c0f7e984ab7aaa63b3ddc592717116bfe2f#body_text
is schema:about of	named entity 'endothelium' named entity 'receptor' named entity 'development' named entity 'advanced' named entity 'dependent' named entity 'platelet activity' named entity 'mechanisms' named entity 'Sciences' named entity 'thrombosis' named entity 'high' named entity 'pulmonary artery' named entity 'masses' named entity 'theory' named entity 'expression' named entity 'procoagulant' named entity 'venous system' named entity 'conditions' named entity 'migration' named entity 'activated' named entity 'function' named entity 'Hypoxia' named entity 'asthma' named entity 'process' named entity 'activation' named entity 'proinflammatory cytokines' named entity 'sickle cell anemia' named entity 'thrombotic complications' named entity 'phenotype' named entity 'Chronic obstructive pulmonary disease' named entity 'downregulation' named entity 'emboli' named entity 'Hypoxia' named entity 'platelet activity' named entity 'thrombotic' named entity 'endothelium' named entity 'proinflammatory cytokines' named entity 'thrombosis' named entity 'Molecular Sciences' named entity 'Thrombosis' named entity 'mechanisms' named entity 'thrombin' named entity 'platelet' named entity 'Thrombotic complications' named entity 'nucleus' named entity 'DVT' named entity 'heterozygous' named entity 'thrombosis' named entity 'influenza virus' named entity 'HIF' named entity 'venous thromboembolism' named entity 'thrombotic events' named entity '10.6' named entity 'platelet' named entity 'thrombi' named entity 'Histones' named entity 'pathophysiological' named entity 'endothelial dysfunction' named entity 'platelets' named entity 'severe injury' named entity 'DVT' named entity 'thrombotic' named entity 'upregulated' named entity 'thrombosis' named entity 'emboli' named entity 'thrombomodulin' named entity 'TFPI' named entity 'megakaryocytes' named entity 'thromboemboli' named entity 'thrombus' named entity 'HIFs' named entity 'metabolically active'

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