進行性腎線維化にはたすMCP‐1‐CCR2の役割と治療戦略への応用

  • 和田 隆志
    金沢大学大学院医学系研究科腎臓内科 金沢大学医学部附属病院血液浄化療法部
  • 横山 仁
    金沢大学大学院医学系研究科腎臓内科 金沢大学医学部附属病院血液浄化療法部
  • 向田 直史
    金沢大学がん研究所組織分子構築研究分野
  • 松島 綱治
    東京大学大学院医学系研究科分子予防医学

書誌事項

タイトル別名
  • MCP-1-CCR2 in renal fibrosis

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説明

Studies of chemokines and their cognate receptors have shed light on the detailed molecular mechanisms of leukocyte trafficking and activation in various inflammatory diseases including renal ones. Chemokine receptors expressed on renal resident cells might be involved in proliferation, proteinuria and fibrogenesis. Novel biological functions of chemokines would expand their universe beyond chemotaxis and activation of inflammatory cells in renal diseases. Importantly, MCP-1 and its cognate receptor CCR2 are now considered to contribute to progressive renal fibrosis, which is a hallmark of progressive renal diseases despite their etiologies, including diabetic nephropathy. The selective intervention of MCP-1-CCR2 via the administration of anti-MCP-1 neutralizing antibodies, CCR2 antagonists and the MCP-1 mutant ameliorated progressive renal fibrosis by resulting in decrease in the deposit of type I collagen and in reduced expression of TGF-β. This MCP-1-CCR2-dependent loop for progressive renal fibrosis was confirmed in CCR2 gene targeted mice. These findings suggest that the therapeutic strategy of blocking MCP-1-CCR2 may prove beneficial for progressive renal fibrosis.

収録刊行物

  • 炎症・再生

    炎症・再生 24 (5), 567-572, 2004

    一般社団法人 日本炎症・再生医学会

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