Megakaryocyte modification of platelets in thrombocytopenia

Roweth, H. G. ORCID: https://orcid.org/0000-0002-1100-8409, Parvin, S. and Machlus, K. R. ORCID: https://orcid.org/0000-0002-2155-1050 (2018) Megakaryocyte modification of platelets in thrombocytopenia. Current opinion in hematology, 25 (5). pp. 410-415. ISSN 1531-7048 doi: 10.1097/moh.0000000000000451

Abstract/Summary

<h4>Purpose of review</h4>Platelets are small, anucleate cells that circulate within the blood and play essential roles in preserving vascular integrity. However, abnormalities in either platelet production or destruction can result in thrombocytopenia, clinically defined by a platelet count lower than 150 000/μL of whole blood. Thrombocytopenia is frequently associated with impaired hemostatic responses to vascular injury and can be life-threatening because of bleeding complications. Megakaryocytes are the precursor cells responsible for platelet production, a process commonly referred to as thrombopoiesis. This review specifically discusses how perturbation of molecular mechanisms governing megakaryocyte differentiation and development manifest in various forms of thrombocytopenia.<h4>Recent findings</h4>This review highlights the identification of novel transcriptional regulators of megakaryocyte maturation and platelet production. We also provide an update into the essential role of cytoskeletal regulation in thrombopoiesis, and how both megakaryopoiesis and platelet production are altered by anticancer therapeutics. Lastly, we focus on recent investigative approaches to treat thrombocytopenia and discuss future prospects in the field of megakaryocyte research.<h4>Summary</h4>In patients where thrombocytopenia is not due to heightened platelet destruction or clearance, defects in megakaryocyte development should be considered.

Item Type	Article
URI	https://centaur.reading.ac.uk/id/eprint/127730
Identification Number/DOI	10.1097/moh.0000000000000451
Refereed	Yes
Divisions	No Reading authors. Back catalogue items
Publisher	Lippincott, Williams & Wilkins
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