Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Feb 24;10(5):894.
doi: 10.3390/jcm10050894.

Thrombocytopathies: Not Just Aggregation Defects-The Clinical Relevance of Procoagulant Platelets

Alessandro Aliotta  1 , Debora Bertaggia Calderara  1 , Maxime G Zermatten  1 , Matteo Marchetti  1   2 , Lorenzo Alberio  1
Affiliations
Review

Thrombocytopathies: Not Just Aggregation Defects-The Clinical Relevance of Procoagulant Platelets

Alessandro Aliotta et al. J Clin Med. .

Abstract

Platelets are active key players in haemostasis. Qualitative platelet dysfunctions result in thrombocytopathies variously characterized by defects of their adhesive and procoagulant activation endpoints. In this review, we summarize the traditional platelet defects in adhesion, secretion, and aggregation. In addition, we review the current knowledge about procoagulant platelets, focusing on their role in bleeding or thrombotic pathologies and their pharmaceutical modulation. Procoagulant activity is an important feature of platelet activation, which should be specifically evaluated during the investigation of a suspected thrombocytopathy.

Keywords: activation endpoints; platelet disorders; procoagulant platelets; thrombocytopathy.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Principal Activation Endpoints During Platelet Activation. At first, platelet receptors interact with adhesive agonists exposed at the site of lesion: von Willebrand factor (VWF) binds to glycoprotein (GP) Ib-IX-V complex and collagen interacts with integrin α2β1 for adhesion and GPVI to mediate platelet activation. These first interactions initiate platelet response. Soluble agonists released by either activated platelets or injured tissue amplify platelet response and activation. These agonists induce proper receptor activation and their signalling converge to activate a core set of intracellular signalling pathways leading to various activation endpoints, such as shape change and formation of pseudopodia, secretion of α-granule and dense granule content, activation of GPIIb/IIIa sustaining platelet aggregation, and externalization of negatively charged amino-phospholipids, contributing to platelet procoagulant activity (thrombin generation).
See this image and copyright information in PMC

References

    1. Quach M.E., Chen W., Li R. Mechanisms of platelet clearance and translation to improve platelet storage. Blood. 2018;131:1512–1521. doi: 10.1182/blood-2017-08-743229. - DOI - PMC - PubMed
    1. Jobe S.M., Di Paola J. Consultative Hemostasis and Thrombosis. Elsevier; Amsterdam, The Netherlands: 2019. Congenital and acquired disorders of platelet function and number; pp. 145–166.
    1. Shen Y.M., Frenkel E.P. Acquired platelet dysfunction. Hematol. Oncol. Clin. North. Am. 2007;21:647–661. doi: 10.1016/j.hoc.2007.06.001. - DOI - PubMed
    1. Cherry-Bukowiec J., Napolitano L. Evidence-Based Practice of Critical Care. Elsevier; Amsterdam, The Netherlands: 2010. What platelet disorders occur in the intensive care unit and how should they be treated? pp. 645–660.
    1. Bye A.P., Unsworth A.J., Gibbins J.M. Platelet signaling: A complex interplay between inhibitory and activatory networks. J. Thromb. Haemost. 2016;14:918–930. doi: 10.1111/jth.13302. - DOI - PMC - PubMed

LinkOut - more resources