Inhibition of ERK1/2 signaling prevents bone marrow fibrosis by reducing osteopontin plasma levels in a myelofibrosis mouse model

• Published in: Leukemia Vol. 37; no. 5; pp. 1068 - 1079
• Main Authors: Bianchi, Elisa, Rontauroli, Sebastiano, Tavernari, Lara, Mirabile, Margherita, Pedrazzi, Francesca, Genovese, Elena, Sartini, Stefano, Dall’Ora, Massimiliano, Grisendi, Giulia, Fabbiani, Luca, Maccaferri, Monica, Carretta, Chiara, Parenti, Sandra, Fantini, Sebastian, Bartalucci, Niccolò, Calabresi, Laura, Balliu, Manjola, Guglielmelli, Paola, Potenza, Leonardo, Tagliafico, Enrico, Losi, Lorena, Dominici, Massimo, Luppi, Mario, Vannucchi, Alessandro Maria, Manfredini, Rossella
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.05.2023; Nature Publishing Group
• Subjects: 14/63; 38/77; 38/79; 631/67/1990/2331; 631/80/86; 64/60; 692/420; 82/80; 96/1; 96/106; 96/95; Animals; Antibodies; Bone marrow; Cancer Research; Cell proliferation; Collagen; Critical Care Medicine; Disease Models, Animal; Extracellular signal-regulated kinase; Fibrosis; Fibrosis - drug therapy; Hematology; Humans; Intensive; Internal Medicine; Medicine; Medicine & Public Health; Mice; Myelofibrosis; Myeloproliferation; Neutralization; Oncology; Osteopontin; Osteopontin - antagonists & inhibitors; Osteopontin - blood; Osteopontin - metabolism; Plasma levels; Primary Myelofibrosis - drug therapy; Primary Myelofibrosis - metabolism; Primary Myelofibrosis - pathology; Signal Transduction - drug effects; Stromal cells

Clonal myeloproliferation and development of bone marrow (BM) fibrosis are the major pathogenetic events in myelofibrosis (MF). The identification of novel antifibrotic strategies is of utmost importance since the effectiveness of current therapies in reverting BM fibrosis is debated. We previously...