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.
Keywords: Coagulopathy; Endothelium; Platelets; SARS-CoV-2; Selenium.
【저자키워드】 SARS-CoV-2, Platelets, Endothelium, Coagulopathy, Selenium, 【초록키워드】 Critical illness, platelet activation, immune response, Platelets, Endothelium, Coagulopathy, Selenium, epidemiological, latency, Critical, mechanism, homeostasis, Evidence, Perturbation, endothelial, perturbations, impairment, physiological functions, complication of COVID-19, COVID 19 patients, transcriptomic, selenocysteine, Taking, COVID 19 patient, 【제목키워드】 COVID-19 patient,