@article{oai:kanazawa-u.repo.nii.ac.jp:00013382,
 author = {Wada, Takashi and Sakai, Norihiko and Sakai, Yoshio and Matsushima, Kouji and Kaneko, Shuichi and Furuichi, Kengo},
 issue = {1},
 journal = {Clinical and Experimental Nephrology},
 month = {Feb},
 note = {Cellular mechanisms have been proposed in the pathogenesis of fibrotic processes in the kidney. In this setting, cell sources underlying the generation of matrix-producing cells in diseased kidneys have been categorized as activated resident stromal cells (e.g., fibroblasts, pericytes), infiltrating bone-marrow-derived cells (e.g., fibrocytes, T cells, macrophages), and cells derived from epithelial-mesenchymal transition/endothelial-mesenchymal transition. Among these cell sources, accumulating evidence has shed light on the involvement of bone-marrow-derived cells, including monocytes/macrophages, and a circulating mesenchymal progenitor cell, fibrocyte, in the progression of fibrosis in kidney. Bone-marrow-derived cells positive for CD45 or CD34, and type 1 (pro)collagen dependent on the chemokine and renin-angiotensin systems migrate into diseased kidneys and enhance synthesis matrix protein, cytokines/chemokines, and profibrotic growth factors, which may promote and escalate chronic inflammatory processes and possible interaction with resident stromal cells, thereby perpetuating kidney fibrosis. © 2010 Japanese Society of Nephrology., 金沢大学医薬保健研究域医学系},
 pages = {8--13},
 title = {Involvement of bone-marrow-derived cells in kidney fibrosis},
 volume = {15},
 year = {2011}
}