| Literature DB >> 33477816 |
Mariarita Spampinato1, Cesarina Giallongo2, Alessandra Romano3, Lucia Longhitano1, Enrico La Spina3, Roberto Avola1, Grazia Scandura3, Ilaria Dulcamare3, Vincenzo Bramanti4, Michelino Di Rosa5, Nunzio Vicario6, Rosalba Parenti6, Giovanni Li Volti1, Daniele Tibullo1, Giuseppe A Palumbo2.
Abstract
Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hematopoietic stem-cell-derived clonal proliferation, leading to bone marrow (BM) fibrosis. Hematopoiesis alterations are closely associated with modifications of the BM microenvironment, characterized by defective interactions between vascular and endosteal niches. As such, neoangiogenesis, megakaryocytes hyperplasia and extensive bone marrow fibrosis, followed by osteosclerosis and bone damage, are the most relevant consequences of PMF. Moreover, bone tissue deposition, together with progressive fibrosis, represents crucial mechanisms of disabilities in patients. Although the underlying mechanisms of bone damage observed in PMF are still unclear, the involvement of cytokines, growth factors and bone marrow microenvironment resident cells have been linked to disease progression. Herein, we focused on the role of megakaryocytes and their alterations, associated with cytokines and chemokines release, in modulating functions of most of the bone marrow cell populations and in creating a complex network where impaired signaling strongly contributes to progression and disabilities.Entities:
Keywords: bone; bone marrow; fibrosis; myeloproliferative neoplasm; primary myelofibrosis
Year: 2021 PMID: 33477816 PMCID: PMC7832894 DOI: 10.3390/biom11010122
Source DB: PubMed Journal: Biomolecules ISSN: 2218-273X