Van Goor H, Ding G, Kees-Folts D, Grond J, Schreiner G F, Diamond J R
Department of Pathology, University of Groningen, The Netherlands.
Lab Invest. 1994 Oct;71(4):456-64.
In this multimodel overview, we have provided the seminal experimental evidence for the crucial contribution of macrophages in the progression of glomerular and interstitial fibrosis. Although all the experimental data provided in this review definitely increase our understanding of the progress of renal disease, we have been mindful to use caution in extrapolating data from animal experiments to the clinical setting (109). In addition, uncertainty still exists as to whether macrophages activation entails a generalized mechanism in which the cells release growth factors and other mediators such as bioactive lipids and nitric oxide simultaneously, or a selective mechanism in which the cells release some but not all macrophage products (110). However, we anticipate that further substantial clinical and experimental observations are on the horizon. Novel therapeutic strategies in these models must be concerned with the prevention of renal macrophage recruitment and/or the suppression of the fibrogenic ability of this pluripotential inflammatory cell.
在本多模型综述中，我们提供了开创性的实验证据，证明巨噬细胞在肾小球和间质纤维化进展中起关键作用。尽管本综述中提供的所有实验数据无疑加深了我们对肾脏疾病进展的理解，但我们在将动物实验数据外推至临床情况时一直谨慎行事（109）。此外，关于巨噬细胞激活是涉及一种普遍机制，即细胞同时释放生长因子和其他介质（如生物活性脂质和一氧化氮），还是一种选择性机制，即细胞仅释放部分而非全部巨噬细胞产物，仍存在不确定性（110）。然而，我们预计即将有更多重要的临床和实验观察结果出现。这些模型中的新型治疗策略必须关注预防肾脏巨噬细胞募集和/或抑制这种多能炎症细胞的促纤维化能力。
