Division of Nephrology, Department of Laboratory Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Clin Exp Nephrol. 2011 Feb;15(1):8-13. doi: 10.1007/s10157-010-0372-2. Epub 2010 Dec 10.
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.
细胞机制已被提出是肾脏纤维化过程发病机制的基础。在这种情况下，疾病肾脏中产生基质产生细胞的细胞来源可分为激活的固有基质细胞（例如成纤维细胞、周细胞）、浸润的骨髓来源细胞（例如纤维母细胞、T 细胞、巨噬细胞）和来源于上皮-间充质转化/内皮-间充质转化的细胞。在这些细胞来源中，越来越多的证据表明骨髓来源的细胞，包括单核细胞/巨噬细胞和循环间充质祖细胞纤维母细胞，参与了肾脏纤维化的进展。对趋化因子和肾素-血管紧张素系统依赖的 CD45 或 CD34 阳性的骨髓来源细胞和 1 型（原）胶原迁移到病变肾脏中，并增强基质蛋白、细胞因子/趋化因子和促纤维化生长因子的合成，这可能促进和加剧慢性炎症过程，并可能与固有基质细胞相互作用，从而使肾脏纤维化持续存在。
