Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.
Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.
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DOI：
10.1038/nrneph.2015.3
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发表时间：
2015-05
影响因子：
41.5
通讯作者：
Bonventre, Joseph V.
中科院分区：
文献类型：
--
作者：
Ferenbach, David A.;Bonventre, Joseph V.
急性肾损伤是一种越来越常见的住院并发症，并与高水平的发病率和死亡率相关。水肿、脓毒性或毒性损伤可引发一系列事件，导致微循环受损、炎症途径激活和肾小管细胞损伤或死亡。这些过程最终导致肾功能急性受损并启动修复反应。这篇综述探讨了急性肾损伤的启动和传播的各种机制，严重受损的肾脏可以再生其正常结构的原型机制，以及自适应修复过程如何变得适应不良。这些机制包括G2/M细胞周期停滞、细胞衰老、促纤维化细胞因子产生以及周细胞和间质肌成纤维细胞的活化，有助于进展性纤维化肾病的发展。最终的结果是一种模拟肾脏加速老化的状态。这些机制为设计靶向治疗策略提供了重要机会，以促进适应性肾脏恢复并最大限度地减少急性损伤后进行性纤维化和慢性肾脏疾病。
Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired microcirculation, activation of inflammatory pathways and tubular cell injury or death. These processes ultimately result in acutely impaired kidney function and initiation of a repair response. This Review explores the various mechanisms responsible for the initiation and propagation of acute kidney injury, the prototypic mechanisms by which a substantially damaged kidney can regenerate its normal architecture, and how the adaptive processes of repair can become maladaptive. These mechanisms, which include G2/M cell-cycle arrest, cell senescence, profibrogenic cytokine production, and activation of pericytes and interstitial myofibroblasts, contribute to the development of progressive fibrotic kidney disease. The end result is a state that mimics accelerated kidney ageing. These mechanisms present important opportunities for the design of targeted therapeutic strategies to promote adaptive renal recovery and minimize progressive fibrosis and chronic kidney disease after acute insults.
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影响因子：
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DOI：
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