MCP-1-CCR2 in renal fibrosis

DOI 29 References
  • Wada Takashi
    Department of Gastroenterology and Nephrology, Kanazawa University Graduate School of Medical Science Division of Blood Purification, Kanazawa University Hospital
  • Yokoyama Hitoshi
    Department of Gastroenterology and Nephrology, Kanazawa University Graduate School of Medical Science Division of Blood Purification, Kanazawa University Hospital
  • Mukaida Naofumi
    Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University
  • Matsushima Kouji
    Depratment of Molecular Prevent Medicine, Graduate School of medicine, University of Tokyo

Bibliographic Information

Other Title
  • 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

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Description

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.

Journal

  • Ensho Saisei

    Ensho Saisei 24 (5), 567-572, 2004

    The Japanese Society of Inflammation and Regeneration

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