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Mediterr J Hematol Infect Dis. 2018 Nov 1;10(1):e2018068. doi: 10.4084/MJHID.2018.068. eCollection 2018.

Megakaryocyte Contribution to Bone Marrow Fibrosis: many Arrows in the Quiver.

Author information

1
Department of Molecular Medicine, University of Pavia, Pavia, Italy.
2
Biotechnology Research Laboratories, IRCCS San Matteo Foundation, Pavia, Italy.
3
Unit of Microscopic and Ultrastructural Anatomy, Department of Medicine, University Campus Bio-Medico, Rome, Italy.
4
Department of Biomedical and Neuromotorial Sciences, Alma Mater University, Bologna, Italy.
5
Department of Biomedical Engineering, Tufts University, Medford, MA, USA.

Abstract

In Primary Myelofibrosis (PMF), megakaryocyte dysplasia/hyperplasia determines the release of inflammatory cytokines that, in turn, stimulate stromal cells and induce bone marrow fibrosis. The pathogenic mechanism and the cells responsible for progression to bone marrow fibrosis in PMF are not completely understood. This review article aims to provide an overview of the crucial role of megakaryocytes in myelofibrosis by discussing the role and the altered secretion of megakaryocyte-derived soluble factors, enzymes and extracellular matrices that are known to induce bone marrow fibrosis.

KEYWORDS:

Bone marrow; Fibrosis; Megakaryocyte; Myeloproliferative neoplasms; Platelets; Transforming growth factor-β

Conflict of interest statement

Competing interests: The authors have declared that no competing interests exist.

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