| dc.creator | Vavougios G.D., Ntoskas K.T., Doskas T.K. | en |
| dc.date.accessioned | 2023-01-31T10:30:37Z | |
| dc.date.available | 2023-01-31T10:30:37Z | |
| dc.date.issued | 2021 | |
| dc.identifier | 10.1016/j.mehy.2020.110475 | |
| dc.identifier.issn | 03069877 | |
| dc.identifier.uri | http://hdl.handle.net/11615/80536 | |
| dc.description.abstract | Coagulopathy 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 Ltd | en |
| dc.language.iso | en | en |
| dc.source | Medical Hypotheses | en |
| dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85098865551&doi=10.1016%2fj.mehy.2020.110475&partnerID=40&md5=6d6e93bc6c3bfeb5da7c3f6817f053f4 | |
| dc.subject | selenium | en |
| dc.subject | selenocysteine | en |
| dc.subject | selenoprotein | en |
| dc.subject | selenium | en |
| dc.subject | selenocysteine | en |
| dc.subject | transcriptome | en |
| dc.subject | amino acid synthesis | en |
| dc.subject | Article | en |
| dc.subject | blood clotting disorder | en |
| dc.subject | coronavirus disease 2019 | en |
| dc.subject | critical illness | en |
| dc.subject | diet supplementation | en |
| dc.subject | disease association | en |
| dc.subject | human | en |
| dc.subject | immune dysregulation | en |
| dc.subject | immune response | en |
| dc.subject | immunomodulation | en |
| dc.subject | nonhuman | en |
| dc.subject | selenium deficiency | en |
| dc.subject | Severe acute respiratory syndrome coronavirus 2 | en |
| dc.subject | thrombocyte activation | en |
| dc.subject | transcriptomics | en |
| dc.subject | virus latency | en |
| dc.subject | biosynthesis | en |
| dc.subject | blood clotting disorder | en |
| dc.subject | chemistry | en |
| dc.subject | complication | en |
| dc.subject | homeostasis | en |
| dc.subject | immune system | en |
| dc.subject | inflammation | en |
| dc.subject | metabolism | en |
| dc.subject | oxidative stress | en |
| dc.subject | pathogenicity | en |
| dc.subject | theoretical model | en |
| dc.subject | thrombocyte | en |
| dc.subject | vascular endothelium | en |
| dc.subject | virology | en |
| dc.subject | Blood Coagulation Disorders | en |
| dc.subject | Blood Platelets | en |
| dc.subject | COVID-19 | en |
| dc.subject | Critical Illness | en |
| dc.subject | Endothelium, Vascular | en |
| dc.subject | Homeostasis | en |
| dc.subject | Humans | en |
| dc.subject | Immune System | en |
| dc.subject | Inflammation | en |
| dc.subject | Models, Theoretical | en |
| dc.subject | Oxidative Stress | en |
| dc.subject | Platelet Activation | en |
| dc.subject | SARS-CoV-2 | en |
| dc.subject | Selenium | en |
| dc.subject | Selenocysteine | en |
| dc.subject | Transcriptome | en |
| dc.subject | Churchill Livingstone | en |
| dc.title | Impairment in selenocysteine synthesis as a candidate mechanism of inducible coagulopathy in COVID-19 patients | en |
| dc.type | journalArticle | en |