2023 Fiscal Year Final Research Report
A study on the mechanism of pulmonary tissue damage induced by high HMGA2 expression in myelodysplastic syndromes
| Project/Area Number |
21K07073
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 49070:Immunology-related
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | 骨髄異形成症候群 / HMGA2 |
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| Outline of Final Research Achievements |
Myelodysplastic syndromes (MDS) often involve complications such as noninfectious pneumonia and autoimmune diseases. HMGA2 is known as a factor that exacerbates the pathology in hematopoietic neoplasms, and its high expression has been reported in cases of myelofibrosis and MDS. However, the involvement of HMGA2 overexpression in the pathogenesis of MDS was remained unclear. We generated an HMGA2 overexpression MDS model mice that reflects clinical findings. Analyses of this model revealed that HMGA2 overexpression contributes to platelet activation. Activated platelets interact with MDS clone-derived neutrophils, which exhibit increased susceptibility to cell death, thereby contributing to the development of noninfectious pneumonia.
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| Free Research Field |
腫瘍生物学
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| Academic Significance and Societal Importance of the Research Achievements |
MDS患者におこる非感染性肺炎などの合併症は、生活の質を著しく低下させます。本研究をもとに血小板-好中球複合体形成を標的とした新たな治療法が開発されることで、患者の生活の質が向上する可能性があります。また治療が効率化されることで長期的には医療費の削減につながる可能性があります。
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