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本文引用的文献

1
HMGB1 contributes to kidney ischemia reperfusion injury.高迁移率族蛋白 B1 参与肾脏缺血再灌注损伤。
J Am Soc Nephrol. 2010 Nov;21(11):1878-90. doi: 10.1681/ASN.2009101048. Epub 2010 Sep 16.
2
Neutralization of the extracellular HMGB1 released by ischaemic damaged renal cells protects against renal ischaemia-reperfusion injury.缺血性损伤肾细胞释放的细胞外 HMGB1 的中和作用可防止肾缺血再灌注损伤。
Nephrol Dial Transplant. 2011 Feb;26(2):469-78. doi: 10.1093/ndt/gfq466. Epub 2010 Aug 2.
3
RAGE and the pathogenesis of chronic kidney disease.晚期糖基化终末产物受体（RAGE）与慢性肾脏病的发病机制。
Nat Rev Nephrol. 2010 Jun;6(6):352-60. doi: 10.1038/nrneph.2010.54. Epub 2010 Apr 27.
4
Ligands of the receptor for advanced glycation end products, including high-mobility group box 1, limit bacterial dissemination during Escherichia coli peritonitis.晚期糖基化终产物受体的配体，包括高迁移率族蛋白 B1，可限制大肠埃希菌腹膜炎期间细菌的播散。
Crit Care Med. 2010 Jun;38(6):1414-22. doi: 10.1097/CCM.0b013e3181de18bc.
5
Toll-like receptors 2 and 4 in renal ischemia/reperfusion injury. Toll 样受体 2 和 4 在肾缺血/再灌注损伤中的作用。
Pediatr Nephrol. 2010 May;25(5):853-60. doi: 10.1007/s00467-009-1422-4. Epub 2010 Feb 4.
6
Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome.坏死细胞通过 NLRP3 炎性小体引发无菌性炎症反应。
Proc Natl Acad Sci U S A. 2009 Dec 1;106(48):20388-93. doi: 10.1073/pnas.0908698106. Epub 2009 Nov 16.
7
Activation of the NLRP3 inflammasome in dendritic cells induces IL-1beta-dependent adaptive immunity against tumors.树突状细胞中NLRP3炎性小体的激活诱导针对肿瘤的白细胞介素-1β依赖性适应性免疫。
Nat Med. 2009 Oct;15(10):1170-8. doi: 10.1038/nm.2028. Epub 2009 Sep 20.
8
Comparison of distinct protein isoforms of the receptor for advanced glycation end-products expressed in murine tissues and cell lines.在小鼠组织和细胞系中表达的晚期糖基化终产物受体不同蛋白异构体的比较。
Cell Tissue Res. 2009 Jul;337(1):79-89. doi: 10.1007/s00441-009-0791-0. Epub 2009 May 5.
9
Alternative splicing of the murine receptor for advanced glycation end-products (RAGE) gene.小鼠晚期糖基化终末产物受体（RAGE）基因的可变剪接
FASEB J. 2009 Jun;23(6):1766-74. doi: 10.1096/fj.08-117739. Epub 2009 Jan 22.
10
Blockade of receptor for advanced glycation end product attenuates pulmonary reperfusion injury in mice.晚期糖基化终产物受体阻断可减轻小鼠肺再灌注损伤。
J Thorac Cardiovasc Surg. 2008 Dec;136(6):1576-85. doi: 10.1016/j.jtcvs.2008.05.032. Epub 2008 Aug 29.

RAGE 不会导致缺血/再灌注损伤引起的肾损伤和损害。

RAGE does not contribute to renal injury and damage upon ischemia/reperfusion-induced injury.

机构信息

Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

出版信息

J Innate Immun. 2012;4(1):80-5. doi: 10.1159/000334251. Epub 2011 Nov 4.

DOI:10.1159/000334251
PMID:22067944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8336648/
Abstract

The receptor for advanced glycation end products (RAGE) mediates a variety of inflammatory responses in renal diseases, but its role in renal ischemia/reperfusion (I/R) injury is unknown. We showed that during renal I/R, RAGE ligands HMGB1 and S100B are expressed. However, RAGE deficiency does not affect renal injury and function upon I/R-induced injury.

摘要

晚期糖基化终产物受体（RAGE）在肾脏疾病中介导多种炎症反应，但它在肾缺血/再灌注（I/R）损伤中的作用尚不清楚。我们发现，在肾 I/R 期间，RAGE 配体 HMGB1 和 S100B 表达。然而，RAGE 缺乏并不影响 I/R 诱导损伤后的肾损伤和功能。