Interaction between systemic inflammation and renal tubular epithelial cells

被引：94
|
作者：
Cantaluppi, Vincenzo [1 ]
Quercia, Alessandro Domenico [1 ]
Dellepiane, Sergio [1 ]
Ferrario, Silvia [1 ]
Camussi, Giovanni [1 ]
Biancone, Luigi [1 ]
机构：
[1] Univ Turin, Dept Med Sci, Dialysis & Kidney Transplantat Unit, Turin, Italy
来源：
NEPHROLOGY DIALYSIS TRANSPLANTATION | 2014年 / 29卷 / 11期
关键词：
acute kidney injury; chronic kidney disease; inflammation; mediators; tubular cells; ACUTE KIDNEY INJURY; ISCHEMIA-REPERFUSION INJURY; INDOXYL SULFATE; MEDIATED REJECTION; IMMUNE-RESPONSES; PATHOPHYSIOLOGY; FAILURE; MICE; ACTIVATION; EXPRESSION;
D O I：
10.1093/ndt/gfu046
中图分类号：
R3 [基础医学]; R4 [临床医学];
学科分类号：
1001 ; 1002 ; 100602 ;
摘要：
Systemic inflammation is known to target tubular epithelial cells (TECs), leading to acute kidney injury. Tubular cells have been implicated in the response to inflammatory mediators in ischaemic and septic renal damage. Moreover, loss of tubular cells by apoptosis or epithelial-to-mesenchymal transition may ingenerate conditions that lead to progression towards chronic kidney disease. On the other hand, TECs may actively contribute to the production of inflammatory mediators that may propagate the injury locally or in distant organs. In the present review, we discuss the tubular cell response and its contribution to systemic inflammation.
引用
收藏
页码：2004 / 2011
页数：8
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