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本文引用的文献

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DNA methylation protects against cisplatin-induced kidney injury by regulating specific genes, including interferon regulatory factor 8.DNA 甲基化通过调节干扰素调节因子 8 等特定基因来防止顺铂引起的肾损伤。
Kidney Int. 2017 Nov;92(5):1194-1205. doi: 10.1016/j.kint.2017.03.038. Epub 2017 Jul 12.
2
Inhibition of HDAC6 protects against rhabdomyolysis-induced acute kidney injury.抑制HDAC6可预防横纹肌溶解诱导的急性肾损伤。
Am J Physiol Renal Physiol. 2017 Mar 1;312(3):F502-F515. doi: 10.1152/ajprenal.00546.2016. Epub 2017 Jan 4.
3
Impact of Transient and Persistent Acute Kidney Injury on Chronic Kidney Disease Progression and Mortality after Gastric Surgery for Gastric Cancer.短暂性和持续性急性肾损伤对胃癌胃切除术后慢性肾脏病进展及死亡率的影响
PLoS One. 2016 Dec 9;11(12):e0168119. doi: 10.1371/journal.pone.0168119. eCollection 2016.
4
Signaling Crosstalk between Tubular Epithelial Cells and Interstitial Fibroblasts after Kidney Injury.肾损伤后肾小管上皮细胞与间质成纤维细胞之间的信号串扰
Kidney Dis (Basel). 2016 Oct;2(3):136-144. doi: 10.1159/000446336. Epub 2016 May 21.
5
Indoxyl Sulfate Enhance the Hypermethylation of Klotho and Promote the Process of Vascular Calcification in Chronic Kidney Disease.硫酸吲哚酚增强Klotho基因的高甲基化并促进慢性肾脏病血管钙化进程。
Int J Biol Sci. 2016 Sep 15;12(10):1236-1246. doi: 10.7150/ijbs.15195. eCollection 2016.
6
Rapid Occurrence of Chronic Kidney Disease in Patients Experiencing Reversible Acute Kidney Injury after Cardiac Surgery.心脏手术后经历可逆性急性肾损伤的患者慢性肾脏病的快速发生
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The duration of acute kidney injury after cardiac surgery increases the risk of long-term chronic kidney disease.心脏手术后急性肾损伤的持续时间会增加长期患慢性肾病的风险。
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Rhein reverses Klotho repression via promoter demethylation and protects against kidney and bone injuries in mice with chronic kidney disease.瑞因通过启动子去甲基化逆转 Klotho 的抑制作用,并预防慢性肾脏病小鼠的肾脏和骨骼损伤。
Kidney Int. 2017 Jan;91(1):144-156. doi: 10.1016/j.kint.2016.07.040. Epub 2016 Sep 28.
9
Progression of Chronic Kidney Disease After Acute Kidney Injury: Role of Self-Perpetuating Versus Hemodynamic-Induced Fibrosis.急性肾损伤后慢性肾脏病的进展:自我延续性纤维化与血流动力学诱导性纤维化的作用
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10
Curcumin attenuates cyclosporine A‑induced renal fibrosis by inhibiting hypermethylation of the klotho promoter.姜黄素通过抑制klotho启动子的高甲基化减轻环孢素A诱导的肾纤维化。
Mol Med Rep. 2016 Oct;14(4):3229-36. doi: 10.3892/mmr.2016.5601. Epub 2016 Aug 8.

AKI 与 CKD:损伤加重、修复受抑,以及潜在机制。

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

机构信息

Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.

Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, Georgia, USA.

出版信息

Kidney Int. 2017 Nov;92(5):1071-1083. doi: 10.1016/j.kint.2017.06.030. Epub 2017 Sep 8.

DOI:10.1016/j.kint.2017.06.030
PMID:28890325
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5683166/
Abstract

Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected. Although AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in patients with CKD, 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 transforming growth factor-β, p53, hypoxia-inducible factor, 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 pathologic changes may contribute to the heightened sensitivity of, and nonrecovery from, AKI in patients with CKD.

摘要

急性肾损伤 (AKI) 和慢性肾脏病 (CKD) 相互关联。虽然 AKI 向 CKD 的转变已得到深入研究,但有关 CKD 中 AKI 的信息却非常有限。尽管如此,当 CKD 患者发生 AKI 时,其病情通常更为严重且难以恢复。CKD 与肾脏组织中细胞信号的显著变化相关,包括转化生长因子-β、p53、缺氧诱导因子和主要发育途径的激活。在细胞水平上,CKD 的特征是线粒体功能障碍、氧化应激和异常自噬。在组织水平上,CKD 的特征是慢性炎症和血管功能障碍。这些病理变化可能导致 CKD 患者 AKI 的敏感性增加和无法恢复。