Progression of chronic kidney disease: too much cellular talk causes damage.
Progression of chronic kidney disease: too much cellular talk causes damage.
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DOI：
10.1016/j.kint.2016.08.025
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发表时间：
2017-03
影响因子：
19.6
通讯作者：
Pozzi A
中科院分区：
文献类型：
--
作者：
Gewin L;Zent R;Pozzi A
肾小管间质纤维化、肾小管萎缩和肾小管周围毛细血管稀疏是慢性肾脏疾病的主要标志。肾小管上皮细胞由多种细胞成分组成，包括肾小管上皮细胞、间充质细胞（成纤维细胞和周细胞）、内皮细胞和炎性细胞。这些细胞成分之间的相互作用是这种复杂疾病发病机制的关键组成部分。在严重或复发性损伤后，肾小管上皮细胞经历结构和细胞周期的变化，伴随着细胞因子的表达和产生的改变。这些细胞因子通过促进成纤维细胞的活化、炎性细胞的募集和内皮细胞的损失而促成纤维化反应的起始。本文综述了生长因子和细胞因子的产生是如何诱导上皮细胞与肾小管细胞的相互作用，从而促进肾损伤后肾小管间质纤维化的进展。
Tubulointerstitial fibrosis, tubular atrophy and peritubular capillary rarefaction are major hallmarks of chronic kidney disease. The tubulointerstitium consists of multiple cell components including tubular epithelia, mesenchymal (fibroblasts and pericytes), endothelial, and inflammatory cells. Crosstalk among these cell components is a key component in the pathogenesis of this complex disease. Following severe or recurrent injury, the renal tubular epithelial cells undergo changes in structure and cell cycle which are accompanied by altered expression and productions of cytokines. These cytokines contribute to the initiation of the fibrotic response by favoring activation of fibroblasts, recruitment of inflammatory cells, and loss of endothelial cells. This review focuses on how augmented growth factor and cytokine production induces epithelial crosstalk with cells in the interstitium to promote progressive tubulointerstitial fibrosis after renal injury.