Εμφάνιση απλής εγγραφής

dc.creatorVavougios G.D., Ntoskas K.T., Doskas T.K.en
dc.date.accessioned2023-01-31T10:30:37Z
dc.date.available2023-01-31T10:30:37Z
dc.date.issued2021
dc.identifier10.1016/j.mehy.2020.110475
dc.identifier.issn03069877
dc.identifier.urihttp://hdl.handle.net/11615/80536
dc.description.abstractCoagulopathy has recently been recognized as a recurring complication of COVID-19, most typically associated with critical illness. There are epidemiological, mechanistic and transcriptomic evidence that link Selenium with SARS-CoV-2's intracellular latency. Taking into consideration the vital role of selenoproteins in maintaining an adequate immune response, endothelial homeostasis and a non-prothrombotic platelet activation status, we propose that impairment in selenocysteine synthesis, via perturbations in the aforementioned physiological functions, potentially constitutes a mechanism of coagulopathy in COVID 19 patients other than those developed in critical illness. © 2020 Elsevier Ltden
dc.language.isoenen
dc.sourceMedical Hypothesesen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85098865551&doi=10.1016%2fj.mehy.2020.110475&partnerID=40&md5=6d6e93bc6c3bfeb5da7c3f6817f053f4
dc.subjectseleniumen
dc.subjectselenocysteineen
dc.subjectselenoproteinen
dc.subjectseleniumen
dc.subjectselenocysteineen
dc.subjecttranscriptomeen
dc.subjectamino acid synthesisen
dc.subjectArticleen
dc.subjectblood clotting disorderen
dc.subjectcoronavirus disease 2019en
dc.subjectcritical illnessen
dc.subjectdiet supplementationen
dc.subjectdisease associationen
dc.subjecthumanen
dc.subjectimmune dysregulationen
dc.subjectimmune responseen
dc.subjectimmunomodulationen
dc.subjectnonhumanen
dc.subjectselenium deficiencyen
dc.subjectSevere acute respiratory syndrome coronavirus 2en
dc.subjectthrombocyte activationen
dc.subjecttranscriptomicsen
dc.subjectvirus latencyen
dc.subjectbiosynthesisen
dc.subjectblood clotting disorderen
dc.subjectchemistryen
dc.subjectcomplicationen
dc.subjecthomeostasisen
dc.subjectimmune systemen
dc.subjectinflammationen
dc.subjectmetabolismen
dc.subjectoxidative stressen
dc.subjectpathogenicityen
dc.subjecttheoretical modelen
dc.subjectthrombocyteen
dc.subjectvascular endotheliumen
dc.subjectvirologyen
dc.subjectBlood Coagulation Disordersen
dc.subjectBlood Plateletsen
dc.subjectCOVID-19en
dc.subjectCritical Illnessen
dc.subjectEndothelium, Vascularen
dc.subjectHomeostasisen
dc.subjectHumansen
dc.subjectImmune Systemen
dc.subjectInflammationen
dc.subjectModels, Theoreticalen
dc.subjectOxidative Stressen
dc.subjectPlatelet Activationen
dc.subjectSARS-CoV-2en
dc.subjectSeleniumen
dc.subjectSelenocysteineen
dc.subjectTranscriptomeen
dc.subjectChurchill Livingstoneen
dc.titleImpairment in selenocysteine synthesis as a candidate mechanism of inducible coagulopathy in COVID-19 patientsen
dc.typejournalArticleen


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