PDF(Pubmed)
Abstract：
Tubulointerstitial fibrosis (TIF), a common end result of almost all progressive chronic kidney diseases (CKD), is also the best predictor of kidney survival. Almost all cells in the kidney are involved in the progression of TIF. Myofibroblasts, the primary producers of extracellular matrix, have previously received a great deal of attention; however, a large body of emerging evidence reveals that proximal tubule (PT) plays a central role in TIF progression. In response to injury, renal tubular epithelial cells (TECs) transform into inflammatory and fibroblastic cells, producing various bioactive molecules that drive interstitial inflammation and fibrosis. Here we reviewed the increasing evidence for the key role of the PT in promoting TIF in tubulointerstitial and glomerular injury and discussed the therapeutic targets and carrier systems involving the PT that holds particular promise for treating patients with fibrotic nephropathy.
摘要：
肾小管间质纤维化（TIF），几乎所有进行性慢性肾脏疾病（CKD）的共同最终结果，也是肾脏存活的最佳预测因子。肾脏中几乎所有的细胞都参与了TIF的进展。肌成纤维细胞,细胞外基质的初级生产者，以前受到了很多关注；然而，大量新出现的证据表明，近端小管（PT）在TIF进展中起着重要作用。为了应对伤害，肾小管上皮细胞（TECs）转化为炎症和成纤维细胞，产生驱动间质炎症和纤维化的各种生物活性分子。在这里，我们回顾了越来越多的证据，表明PT在促进TIF在肾小管间质和肾小球损伤中的关键作用，并讨论了涉及PT的治疗靶标和载体系统，这对于治疗纤维化肾病患者具有特别的希望。
