Pathophysiology of AKI: Injury and Normal and Abnormal Repair

Pathophysiology of AKI: Injury and Normal and Abnormal Repair
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DOI:
10.1159/000313738
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发表时间:
2010-01-01
期刊:
CARDIORENAL SYNDROMES IN CRITICAL CARE
影响因子:
--
通讯作者:
Bonventre, Joseph V.
Bonventre, Joseph V.
中科院分区:
其他
文献类型:
--
作者:
Bonventre, Joseph V.

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急性肾损伤的病理生理学涉及血管、肾小管和炎症因子之间复杂的相互作用,随后是一个修复过程,该过程既可以使上皮分化和功能恢复正常,也可能导致进行性纤维化的慢性肾脏病。先天性和获得性免疫在损伤阶段、炎症反应的调节以及与上皮层修复相关的过程中都起着重要作用。近期数据改变了对上皮在纤维化中作用的关注方向,并将成肌纤维细胞的产生归因于血管周围和间质的成纤维细胞。上皮通过最近确定的上皮细胞周期停滞与促纤维化细胞因子产生之间的联系,在异常修复中起着重要作用。版权所有(C) 2010 S. Karger AG,巴塞尔
The pathophysiology of acute kidney injury involves a complex interplay among vascular, tubular, and inflammatory factors followed by a repair process that can either restore epithelial differentiation and function to normal or result in progressive fibrotic chronic kidney disease. Innate and acquired immunity play an important role in the injury phase, in the regulation of the inflammatory response, and in processes related to repair of the epithelial layer. Recent data change the direction of focus of the role of the epithelium in fibrosis and attributes myelofibroblast production to perivascular and interstitial fibroblasts. The epithelium plays an important role in abnormal repair through a recently defined link between cell cycle arrest of the epithelial cell and profibrogenic cytokine production. Copyright (C) 2010 S. Karger AG, Basel