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Updated: Feb 8, 2026
Isolation of Mouse Megakaryocyte Progenitors
Published on: May 20, 2021
Do megakaryocytes contribute to organ fibrosis?
Gerard Gurumurthy1,2, Jecko Thachil3
1The Queen Elizabeth Hospital Kings Lynn NHS Foundation Trust, Kings Lynn, UK.
Abstract:
Megakaryocytes, the platelet precursors, have been known to populate tissues other than the bone marrow, most prominently the lung, but also the liver and spleen. Work in myeloproliferative neoplasms has established that dysplastic megakaryocytes are central organisers of the fibrosis in the bone marrow. In this commentary, we frame a hypothesis-gathering question as to whether megakaryocytes might analogously act as context-dependent contributors to organ fibrosis outside the marrow. In the lung, studies have identified resident/trafficking megakaryocytes with inflammatory properties, while in the liver, megakaryocytes-rich extramedullary foci often co-localise with periportal and perisinusoidal fibrosis. Approved agents for idiopathic pulmonary fibrosis act on broad growth-factor pathways across multiple cell types that may overlapwith the megakaryocytes/platelet secretome. It is thus possible that megakaryocytes may play a contributory role in organ fibrosis. We acknowledge that these observations are associative and preclinical, and that established epithelial-mesenchymal mechanisms remain central in organ fibrosis. We therefore do not assert that megakaryocytes are contributors of organ fibrosis. Rather, we pose this as a testable question prompted by converging yet incomplete evidence.
Insights
Megakaryocytes, platelet precursors, may contribute to organ fibrosis outside the bone marrow. Further research is needed to confirm if these cells play a role in lung and liver fibrosis.
Area of Science:
- Hematology
- Pathology
- Cell Biology
Background:
- Megakaryocytes (platelet precursors) are found in various organs, including the lung, liver, and spleen, beyond the bone marrow.
- Dysplastic megakaryocytes are implicated in bone marrow fibrosis in myeloproliferative neoplasms.
- Existing treatments for idiopathic pulmonary fibrosis target broad growth-factor pathways potentially involving megakaryocytes and platelets.
Purpose of the Study:
- To investigate the potential role of megakaryocytes in contributing to organ fibrosis outside the bone marrow.
- To explore whether megakaryocytes act as context-dependent organizers of fibrosis in organs like the lung and liver.
- To frame a hypothesis-gathering question based on converging preclinical evidence.
Main Methods:
- Review and synthesis of existing preclinical and associative studies.
- Identification of co-localization of megakaryocytes with fibrotic tissue in the liver.
- Observation of resident/trafficking megakaryocytes with inflammatory properties in the lung.
Main Results:
- Megakaryocytes are present in extramedullary sites and are associated with fibrotic foci in the liver.
- Megakaryocytes in the lung exhibit inflammatory properties.
- Potential overlap exists between megakaryocyte/platelet secretomes and pathways targeted by fibrosis treatments.
Conclusions:
- Megakaryocytes may play a contributory role in organ fibrosis, particularly in the lung and liver.
- The observed associations are preclinical and require further investigation.
- Established epithelial-mesenchymal transition mechanisms remain central to organ fibrosis, but megakaryocyte involvement is a testable hypothesis.
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