Dussaule Jean-Claude, Guerrot Dominique, Huby Anne-Cécile, Boffa Jean-Jacques, Chatziantoniou Christos
Unité INSERM 702, Hôpital Tenon, Paris, France et Université Pierre et Marie Curie, Paris, France.
Bull Acad Natl Med. 2009 Dec;193(9):1993-2003; discussion 2003-4.
With the increasing incidence of chronic renal diseases worldwide, there is an urgent need to understand the mechanisms involved in progression of renalfibrosis. Independently of the underlying cause or trigger, progression of renalfibrosis is mainly characterized by excessive synthesis and abnormal accumulation of extracellular matrix proteins in renal mesenchymal cells. These cells are mainly myofibroblasts deriving from phenotypic transformation of a variety of renal cells, including vascular smooth muscle cells, mesangial cells, tubular epithelial cells, endothelial cells, and pericytes. Recent animal studies showing the regression of renal fibrosis during curative therapy suggest that this phenotypic "transition" is reversible. The plasticity of podocytes controlling glomerular filtration may also play a role in the progression/regression of fibrosis in this setting
随着全球慢性肾脏疾病发病率的不断上升,迫切需要了解肾纤维化进展所涉及的机制。无论潜在病因或触发因素如何,肾纤维化的进展主要特征是肾间质细胞中细胞外基质蛋白的过度合成和异常积累。这些细胞主要是肌成纤维细胞,源自多种肾细胞的表型转化,包括血管平滑肌细胞、系膜细胞、肾小管上皮细胞、内皮细胞和周细胞。最近的动物研究表明,在治疗性治疗期间肾纤维化会消退,这表明这种表型“转变”是可逆的。在这种情况下,控制肾小球滤过的足细胞的可塑性也可能在纤维化的进展/消退中起作用