Abstract
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.
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TW is a recipient of a Grant-in-Aid from the Ministry of Education, Science, Sports and Culture in Japan and Takeda Science Foundation.
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Wada, T., Sakai, N., Sakai, Y. et al. Involvement of bone-marrow-derived cells in kidney fibrosis. Clin Exp Nephrol 15, 8–13 (2011). https://doi.org/10.1007/s10157-010-0372-2
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DOI: https://doi.org/10.1007/s10157-010-0372-2