Wada Takashi, Matsushima Kouji, Kaneko Shuichi
Department of Laboratory Medicine, Graduate School of Medical Science Kanazawa University, Kanazawa, Japan.
Front Biosci. 2008 May 1;13:3966-74. doi: 10.2741/2984.
Leukocyte infiltration to glomeruli plays an essential role in the pathogenesis of glomerulonephritis. Pathophysiological roles of chemokines and their cognate receptors have shed light on the detailed molecular mechanisms of leukocyte trafficking and activation both in clinical and experimental settings of glomerulonephritis. Infiltrating leukocytes and glomerular resident cells interact to promote and exacerbate glomerular injury, eventually leading to glomerulosclerosis. Further, recent studies on chemokines have expanded their universe beyond leukocyte migration to glomeruli, to include homeostasis, development and protection of resident cells in glomeruli. New insights into proteinuria have been uncovered by the regulation of chemokine system. The intervention of chemokines and their cognate receptors may have therapeutic potential to slow the progression of glomerulonephritis.
白细胞浸润至肾小球在肾小球肾炎的发病机制中起重要作用。趋化因子及其同源受体的病理生理作用已阐明了在肾小球肾炎的临床和实验环境中白细胞迁移和激活的详细分子机制。浸润的白细胞与肾小球固有细胞相互作用,促进并加剧肾小球损伤,最终导致肾小球硬化。此外,最近关于趋化因子的研究已将其范围从白细胞向肾小球的迁移扩展至包括肾小球固有细胞的稳态、发育和保护。趋化因子系统的调节揭示了蛋白尿的新见解。趋化因子及其同源受体的干预可能具有减缓肾小球肾炎进展的治疗潜力。