期刊文献+

NLRP3炎症小体与腹膜透析患者腹膜纤维化的研究进展 被引量:7

Research Progress of NLRP3 Inflammasomes and Peritoneal Fibrosis in Peritoneal Dialysis Patients
下载PDF
导出
摘要 腹膜透析已逐渐成为终末期肾病患者的首选治疗方法之一,腹膜纤维化所致的超滤衰竭是患者退出腹膜透析的主要原因。Nod样受体蛋白3(NLRP3)炎症小体是一种模式识别受体,其激活可引起强效促炎因子白细胞介素(IL) 1β、IL-18的成熟和释放,在急慢性炎症反应过程及多种非感染性疾病的发生发展中发挥重要作用。NLRP3炎症小体与腹膜透析过程中的急慢性腹膜炎、腹膜纤维化的发生发展密切相关,阐明NLRP3炎症小体与腹膜透析相关腹膜纤维化的调控机制,可为腹膜纤维化的防治提供理论基础。 Peritoneal dialysis has gradually become one of the preferred treatment methods for patients with end-stage renal disease. The ultrafiltration failure caused by peritoneal fibrosis is the main reason for patients to withdraw from peritoneal dialysis. Nod-like receptor protein 3( NLRP3) inflammasome is a kind of pattern recognition receptor,and its activation can induce the maturation and release of potent proinflammatory factors interleukin( IL) 1β and IL-18,which plays an important role in the occurrence and development of acute and chronic inflammatory reactions and a variety of non-infectious diseases. In recent years,it has been found that NLRP3 inflammasome is closely related to the occurrence and development of acute and chronic peritonitis and peritoneal fibrosis in peritoneal dialysis process,so clarification of the regulatory mechanism between the NLRP3 inflammasomes and peritoneal fibrosis in peritoneal dialysis can provide a theoretical basis for the prevention and treatment of peritoneal fibrosis.
作者 胡清华 罗绮媚 钟少鑫 窦献蕊 HU Qinghua;LUO Qimei;ZHONG Shaoxin;DOU Xianrui(Department of Nephrology,Shunde Hospital of Southern Medical University,Foshan 528300,China)
出处 《医学综述》 2019年第6期1047-1051,1057,共6页 Medical Recapitulate
基金 国家自然科学基金(81800674)
关键词 腹膜透析 Nod样受体蛋白3炎症小体 白细胞介素1Β 腹膜纤维化 线粒体 Peritoneal dialysis Nod-like receptor protein 3 inflammasomes Interleukin 1β Peritoneal fibrosis Mitoch ondria
  • 相关文献

参考文献3

二级参考文献14

  • 1Ron D, Walter P. Signal integration in the endoplasmic reticulum unfolded protein response. Nat Rev Mol Cell Biol 2007; 8:519–529.
  • 2Richardson CE, Kooistra T, Kim DH. An essential role for XBP-1 in host protection against immune activation in C. elegans. Nature 2010; 463:1092–1095.
  • 3Kim DH, Feinbaum R, Alloing G, et al. A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity. Science 2002; 297:623–626.
  • 4Troemel ER, Chu SW, Reinke V, Lee SS, Ausubel FM, Kim DH. p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans. PLoS Genet 2006; 2:e183.
  • 5Kaser A, Lee AH, Franke A, et al. XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease. Cell 2008; 134:743–756.
  • 6Salzman NH, Hung K, Haribhai D, et al. Enteric defensins are essential regulators of intestinal microbial ecology. Nat Immunol 2010; 11:76–83.
  • 7Zheng W, Rosenstiel P, Huse K, et al. Evaluation of AGR2 and AGR3 as candidate genes for inflammatory bowel disease. Genes Immun 2006; 7:11–18.
  • 8Zhao F, Edwards R, Dizon D, et al. Disruption of Paneth and goblet cell homeostasis and increased endoplasmic reticulum stress in Agr2-/-mice. Dev Biol 2010; 338:270–279.
  • 9Zhang FR, Huang W, Chen SM, et al. Genomewide association study of leprosy. N Engl J Med 2009; 361:2609–2618.
  • 10Iwakoshi NN, Pypaert M, Glimcher LH. The transcription factor XBP-1 is essential for the development and survival of dendritic cells. J Exp Med 2007; 204:2267–2275.

共引文献37

同被引文献67

二级引证文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部