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内皮细胞在溶血性尿毒症综合征中的作用。

The role of the endothelium in hemolytic uremic syndrome.

作者信息

Zoja C, Morigi M, Remuzzi G

机构信息

Mario Negri Institute for Pharmacological Research, Bergamo, Italy.

出版信息

J Nephrol. 2001 Nov-Dec;14 Suppl 4:S58-62.

PMID:11798147
Abstract

Hemolytic uremic syndrome (HUS), which is the most common cause of acute renal failure in children, is caused by Shiga toxin-producing Escherichia coli infection. This infection leads to renal and other organ microvascular thrombosis. Endothelial injury has been recognized as the trigger event in the development of microangiopathic process. Evidence suggests that leukocyte as well as platelet activation participate in endothelial damage. Intrinsic abnormalities of the complement system may also play a role in HUS.

摘要

溶血尿毒综合征(HUS)是儿童急性肾衰竭最常见的病因,由产志贺毒素大肠杆菌感染所致。这种感染会导致肾脏及其他器官的微血管血栓形成。内皮损伤被认为是微血管病变发展过程中的触发事件。有证据表明,白细胞以及血小板的激活参与了内皮损伤。补体系统的内在异常也可能在溶血尿毒综合征中起作用。

相似文献

1
The role of the endothelium in hemolytic uremic syndrome.内皮细胞在溶血性尿毒症综合征中的作用。
J Nephrol. 2001 Nov-Dec;14 Suppl 4:S58-62.
2
Alternative pathway activation of complement by Shiga toxin promotes exuberant C3a formation that triggers microvascular thrombosis.志贺毒素通过替代途径激活补体促进丰富的 C3a 形成,从而引发微血管血栓形成。
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Shiga toxin-associated hemolytic uremic syndrome: pathophysiology of endothelial dysfunction.志贺毒素相关性溶血尿毒综合征:内皮功能障碍的病理生理学。
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[Hemolytic uremic syndrome caused by enterohaemorrhagic Escherichia coli].肠出血性大肠杆菌所致溶血性尿毒综合征
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New insights into Shiga toxin-mediated endothelial dysfunction in hemolytic uremic syndrome.新型志贺毒素介导的溶血尿毒综合征血管内皮功能障碍研究进展
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Platelet activation in hemolytic uremic syndrome.溶血性尿毒症综合征中的血小板活化
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Hemolytic uremic syndrome: an example of insufficient complement regulation on self-tissue.溶血尿毒综合征:自身组织补体调节不足的一个例子。
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Relative nephroprotection during Escherichia coli O157:H7 infections: association with intravenous volume expansion.大肠杆菌O157:H7感染期间的相对肾脏保护作用:与静脉补液扩容的关系
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New aspects in the pathogenesis of enteropathic hemolytic uremic syndrome.肠病性溶血尿毒综合征发病机制的新进展。
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Shiga toxin triggers endothelial and podocyte injury: the role of complement activation.志贺毒素引发血管内皮细胞和足细胞损伤:补体激活的作用。
Pediatr Nephrol. 2019 Mar;34(3):379-388. doi: 10.1007/s00467-017-3850-x. Epub 2017 Dec 6.

引用本文的文献

1
Action of shiga toxin type-2 and subtilase cytotoxin on human microvascular endothelial cells.志贺毒素 2 型和枯草溶菌素细胞毒素对人微血管内皮细胞的作用。
PLoS One. 2013 Jul 30;8(7):e70431. doi: 10.1371/journal.pone.0070431. Print 2013.
2
Shiga toxin 1 induces on lipopolysaccharide-treated astrocytes the release of tumor necrosis factor-alpha that alter brain-like endothelium integrity.志贺毒素 1 诱导脂多糖处理的星形胶质细胞释放肿瘤坏死因子-α,改变类脑组织内皮细胞的完整性。
PLoS Pathog. 2012;8(3):e1002632. doi: 10.1371/journal.ppat.1002632. Epub 2012 Mar 29.
3
Shiga toxin pathogenesis: kidney complications and renal failure.
志贺毒素发病机制:肾脏并发症和肾衰竭。
Curr Top Microbiol Immunol. 2012;357:105-36. doi: 10.1007/82_2011_172.
4
p38 mitogen-activated protein kinase mediates lipopolysaccharide and tumor necrosis factor alpha induction of shiga toxin 2 sensitivity in human umbilical vein endothelial cells.p38丝裂原活化蛋白激酶介导脂多糖和肿瘤坏死因子α诱导人脐静脉内皮细胞对志贺毒素2的敏感性。
Infect Immun. 2008 Mar;76(3):1115-21. doi: 10.1128/IAI.01300-07. Epub 2007 Dec 17.
5
Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome: emerging insights for vascular integrity.
Curr Infect Dis Rep. 2005 Sep;7(5):319-21. doi: 10.1007/s11908-005-0002-4.
6
Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic uremic syndrome.在溶血性尿毒症综合征中,补体因子H的突变会降低其与C3b和肝素的结合亲和力以及与内皮细胞的表面附着能力。
J Clin Invest. 2003 Apr;111(8):1181-90. doi: 10.1172/JCI16651.