课题基金 / 基金详情

Involvement of Epithelial and endothelial to mesenchymal transition in tissue remolding of rheumatic diseases

Involvement of Epithelial and endothelial to mesenchymal transition in tissue remolding of rheumatic diseases
上皮和内皮向间质转化参与风湿性疾病的组织重塑
批准号:
23591451
负责人:
SAITO Kazuyoshi
金额:
$3.33万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2013

项目摘要

项目成果

SAITO Kazuyoshi的其他基金

相关文献

中文摘要
翻译
本研究旨在阐明EMT和EndoMT在风湿性疾病组织重塑和纤维化中的作用机制,为风湿性疾病的治疗提供新的策略。我们对风湿性疾病(包括类风湿关节炎、系统性硬化症和血管炎)的皮肤、肺和肾组织进行免疫染色。结果,由于内皮细胞增殖,在组织纤维化和血管重塑的显著进展部位观察到肌成纤维细胞增生。免疫染色显示成肌细胞和内皮细胞均表达Wnt10a,提示Wnt10信号通路可能参与风湿性疾病的不可逆重构。这些令人振奋的发现表明,在风湿病中引起不可逆器官损伤的组织重塑等情况下,抑制EndMT/EMT可能是临床治疗转化的一个有希望的靶点。
英文摘要
The aim of this study is to elucidate the mechanism of EMT and EndoMT in tissue remolding and fibrosis of rheumatic diseases and to develop a new treatment strategy for rheumatic diseases. We conducted immune-staining of skin,lung and kidney tissue from rheumatic disease including rheumatoid arthritis, systemic sclerosis and vasculitis. As a result, a hyperplasia of myofibroblast was observed at the site of prominent progression of tissue fibrosis and vascular remodeling due to endothelial dell proliferation. Immuno-staining revealed both the myoblast and endothelial cells express Wnt10a, suggesting signaling through Wnt10 might involvement in irreversible remodeling in rheumatic diseases. These provocative findings suggest that the inhibition of EndMT/EMT may be a promising target for clinical therapeutic translation in settings such as tissue remodeling which cause of irreversible organ damage in rheumatic deseases.
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会议论文
Novel strategies for treatment of rheumatic diseases by Wnt signal blockades
The mechanism of inflammation in autoimmune response during the acute phase of Kawasaki disease.
  • 批准号:
    22790969
  • 项目类别:
    Grant-in-Aid for Young Scientists (B)
  • 资助金额:
    $2.5万
  • 财政年份:
    2010
  • 负责人:
    SAITO Kazuyoshi
  • 依托单位:
A New treatment strategy using analysis of anti-transcriptional factors antibody in connective tissue diseases.
Therapeutic strategy for inflammatory diseases by a novel negative regulatory transcriptional factor of inflammatory cytokines