Dussaule J-C, Chatziantoniou C
INSERM, Unité 702 Paris F-75020, Paris, France.
Cell Death Differ. 2007 Jul;14(7):1343-9. doi: 10.1038/sj.cdd.4402143. Epub 2007 Mar 30.
Over the last years, evidence emerged demonstrating that the progression of renal fibrosis is reversible in experimental models. The present review summarizes the new insights concerning the mechanisms of progression and regression of renal disease and examines this novel evidence under the light of feasibility and transfer to human nephropathies. The involved mechanisms are discussed with particular emphasis on the fibrotic role of vasoactive peptides such as angiotensin II and endothelin, and growth factors such as transforming growth factor beta (TGFbeta). The possibility of regression is introduced by presenting the in vivo efficiency of anti-hypertensive treatments and of systems that antagonize the fibrogenic action of TGFbeta such as bone morphogenic protein-7 (BMP-7) and hepatocyte growth factor. Finally, we provide a brief description of the promising future directions and clinical considerations about the applications of the experimental data to humans.
在过去几年中，有证据表明在实验模型中肾纤维化的进展是可逆的。本综述总结了有关肾脏疾病进展和消退机制的新见解，并根据可行性以及向人类肾病转化的情况审视了这一新证据。文中讨论了相关机制，特别强调了血管活性肽如血管紧张素II和内皮素以及生长因子如转化生长因子β（TGFβ）的纤维化作用。通过介绍抗高血压治疗以及拮抗TGFβ促纤维化作用的系统如骨形态发生蛋白-7（BMP-7）和肝细胞生长因子在体内的效果，引入了消退的可能性。最后，我们简要描述了有前景的未来方向以及关于将实验数据应用于人类的临床考量。
