The impact of platelets on pulmonary microcirculation throughout COVID-19 and its persistent activating factors.

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  • Additional Information
    • Source:
      Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
    • Publication Information:
      Original Publication: [Lausanne : Frontiers Research Foundation]
    • Subject Terms:
    • Abstract:
      Patients with COVID-19 often have hypoxemia, impaired lung function, and abnormal imaging manifestations in acute and convalescent stages. Alveolar inflammation, pulmonary vasculitis, and thromboembolism synergistically damage the blood-air barrier, resulting in increased pulmonary permeability and gas exchange disorders. The incidence of low platelet counts correlates with disease severity. Platelets are also involved in the impairment of pulmonary microcirculation leading to abnormal lung function at different phases of COVID-19. Activated platelets lose the ability to protect the integrity of blood vessel walls, increasing the permeability of pulmonary microvasculature. High levels of platelet activation markers are observed in both mild and severe cases, short and long term. Therefore, the risk of thrombotic events may always be present. Vascular endothelial injury, immune cells, inflammatory mediators, and hypoxia participate in the high reactivity and aggregation of platelets in various ways. Microvesicles, phosphatidylserine (PS), platelets, and coagulation factors are closely related. The release of various cell-derived microvesicles can be detected in COVID-19 patients. In addition to providing a phospholipid surface for the synthesis of intrinsic factor Xase complex and prothrombinase complex, exposed PS also promotes the decryption of tissue factor (TF) which then promotes coagulant activity by complexing with factor VIIa to activate factor X. The treatment of COVID-19 hypercoagulability and thrombosis still focuses on early intervention. Antiplatelet therapy plays a role in relieving the disease, inhibiting the formation of the hypercoagulable state, reducing thrombotic events and mortality, and improving sequelae. PS can be another potential target for the inhibition of hypercoagulable states.
      Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
      (Copyright © 2022 Xiang, Wu, Jing, Liu, Wang, Wang, Novakovic and Shi.)
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    • Contributed Indexing:
      Keywords: COVID-19; antiplatelet; microvesicles; phosphatidylserine; platelet; thrombosis
    • Accession Number:
      0 (Blood Coagulation Factors)
      0 (Coagulants)
      0 (Inflammation Mediators)
      0 (Phosphatidylserines)
      0 (Platelet Aggregation Inhibitors)
      9001-29-0 (Factor X)
      9008-12-2 (Intrinsic Factor)
      9035-58-9 (Thromboplastin)
      EC 3.4.21.21 (Factor VIIa)
    • Publication Date:
      Date Created: 20221017 Date Completed: 20221018 Latest Revision: 20221020
    • Publication Date:
      20221213
    • Accession Number:
      PMC9559186
    • Accession Number:
      10.3389/fimmu.2022.955654
    • Accession Number:
      36248790