Involvement of bone-marrow-derived cells in kidney fibrosis

T Wada, N Sakai, Y Sakai, K Matsushima… - Clinical and …, 2011 - Springer
T Wada, N Sakai, Y Sakai, K Matsushima, S Kaneko, K Furuichi
Clinical and experimental nephrology, 2011Springer
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 (eg, fibroblasts,
pericytes), infiltrating bone-marrow-derived cells (eg, 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 …
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.
Springer