Browsing by Author "Moliterno, Alison R."

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    Clinical applications of thrombopoietin silencing: A possible therapeutic role in COVID-19?
    (Elsevier, 2021-10) Alentado, Vincent J.; Moliterno, Alison R.; Srour, Edward F.; Kacena, Melissa A.; Medicine, School of Medicine
    Thrombopoietin (TPO) is most recognized for its function as the primary regulator of megakaryocyte (MK) expansion and differentiation. MKs, in turn, are best known for their role in platelet production. Research indicates that MKs and platelets play an extensive role in the pathologic thrombosis at sites of high inflammation. TPO, therefore, is a key mediator of thromboinflammation. Silencing of TPO has been shown to decrease platelets levels and rates of pathologic thrombosis in patients with various inflammatory disorders (Barrett et al, 2020; Bunting et al, 1997; Desai et al, 2018; Kaser et al, 2001; Shirai et al, 2019). Given the high rates of thromboinflammmation in the novel coronavirus 2019 (COVID-19), as well as the well-documented aberrant MK activity in affected patients, TPO silencing offers a potential therapeutic modality in the treatment of COVID-19 and other pathologies associated with thromboinflammation. The current review explores the current clinical applications of TPO silencing and offers insight into a potential role in the treatment of COVID-19.
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    Interaction of the inflammatory response and megakaryocytes in COVID-19 infection
    (Elsevier, 2021-09) Battina, Hanisha L.; Alentado, Vincent J.; Srour, Edward F.; Moliterno, Alison R.; Kacena, Melissa A.; Orthopaedic Surgery, School of Medicine
    The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly across the world and has resulted in more than 4.2 million global deaths as of July 30, 2021. For reasons that remain unknown, the coronavirus disease 2019 (COVID-19) clinically manifests itself in various levels of severity, with most patients positive for COVID-19 being asymptomatic or having only mild symptoms. However, clinical studies in severely ill patients have implicated that manifestations of this infection are due in part to abnormal megakaryocyte (MK) behavior. Additionally, COVID-19–associated cytokine storms have been found to induce aberrant MK formation, primarily through interleukin-6 and Janus kinase-signal transducer and activator of transcription signaling. Autopsy reports have revealed significantly higher rates of MKs in the pulmonary and cardiac systems, which may be responsible for the high rate of thrombotic complications and abnormal coagulopathies in patients with severe forms of COVID-19. This review examines MKs and their potential function in the clinical manifestations of SARS-CoV-2 infection.