Signaling through FcγRIIA and the C5a-C5aR pathway mediates platelet hyperactivation in COVID-19.

ABSTRACT: Patients with COVID-19 present with a wide variety of clinical manifestations. Thromboembolic events constitute a significant cause of morbidity and mortality in patients infected with SARS-CoV-2. Severe COVID-19 has been associated with hyperinflammation and pre-existing cardiovascular disease. Platelets are important mediators and sensors of inflammation and are directly affected by cardiovascular stressors. In this report, we found that platelets from severely ill, hospitalized COVID-19 patients exhibit higher basal levels of activation measured by P-selectin surface expression, and have a poor functional reserve upon in vitro stimulation. Correlating clinical features to the ability of plasma from COVID-19 patients to stimulate control platelets identified ferritin as a pivotal

SUBMITTER: Apostolidis SA 

PROVIDER: S-EPMC8109205 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature