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AKI on CKD: heightened injury suppressed repair and the underlying mechanisms

机译:CKD上的AKI:损伤加重修复受抑制以及潜在机制

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摘要

Acute kidney injury (AKI) and chronic kidney disease (CKD) are inter-connected. While AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in CKD patients, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of TGF-β, p53, HIF, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathological changes may contribute to the heightened sensitivity of, and non-recovery from, AKI in CKD patients.
机译:急性肾损伤(AKI)和慢性肾脏病(CKD)是相互联系的。虽然已经对AKI到CKD的过渡进行了深入研究,但是关于CKD的AKI信息非常有限。但是,已知在CKD患者中发生AKI时,AKI更为严重且难以恢复。 CKD与肾脏组织中细胞信号传导的显着变化有关,包括TGF-β,p53,HIF和主要发育途径的激活。在细胞水平上,CKD的特征在于线粒体功能障碍,氧化应激和自噬异常。在组织水平上,CKD的特征是慢性炎症和血管功能障碍。这些病理变化可能会导致CKD患者AKI的敏感性增高或无法恢复。

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