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首页> 外文期刊>American Journal of Physiology >Ablation of Gsa impairs renal tubule proliferation after injury via CDK2/cyclin E
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Ablation of Gsa impairs renal tubule proliferation after injury via CDK2/cyclin E

机译：通过CDK2 / cyclin E损伤后GSA的消融损害肾小管增殖

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摘要

Acute kidney injury (AKI), a common clinical complication that is associated with unacceptably high morbidity and mortality, may gradually develop into chronic kidney disease (CKD) and eventually progress to end-stage renal disease (10, 31, 41, 45). Acute aristolochic acid nephropathy (AAN) and renal ischemia-reperfusion injury are two common animal models used for the study of AKI (12, 38). However, renal tubular epithelial cells (TECs) are the main targets of nephro-toxic drugs and ischemic injury during the development of AKI. Histologically, TEC lesions are characterized by loss of the brush border, loss of cell polarity, and exposure of the basement membrane (1, 30). Therefore, the proliferative capacity of TECs may be a decisive factor in renal repair or the progression of AKI to CKD, because the maladaptive repair process after AKI is the main cause of renal fibrosis (15, 18, 32). During the kidney repair phase, surviving TECs can proliferate and dedifferentiate and eventually replace the injured tubular cells and restore tubular integrity (18). Thus, the proliferation and regeneration of TECs after AKI play a critical role in determining the outcomes of AKI. However, information about the molecular pathways of TEC proliferation after AKI is lacking.
机译：急性肾脏损伤（AKI），一种与不可接受的高发病率和死亡率有关的常见临床并发症，可能逐渐发展成慢性肾病（CKD），最终进入终末期肾病（10,31,41,45）。急性胰抗菌酸肾病（AAN）和肾缺血再灌注损伤是用于研究AKI（12,38）的两种常见的动物模型。然而，肾小管上皮细胞（TECs）是益藻毒性药物和缺血性损伤的主要目标。组织学上，TEC病变的特征在于刷刷边界，细胞极性丧失和基底膜暴露（1,30）。因此，TECs的增殖能力可能是肾脏修复或AKI进展的决定性因素，因为AKI后的不良修复过程是肾纤维化（15,18,32）的主要原因。在肾修复阶段，存活的TECs可以增殖和消化，并最终取代受伤的管状细胞并恢复管状完整性（18）。因此，AKI后TECS的增殖和再生在确定AKI的结果时发挥着关键作用。然而，缺乏后，有关TEC增殖分子途径的信息。

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