自噬异常在炎症性肠病发病机制中的作用

被引：4

作者：

张琮 ^{[1
]}

陈颖伟 ^{[1
,2
]}

机构：

[1] 上海交通大学医学院附属新华医院消化内科

[2] 上海市小儿消化与营养重点实验室

来源：

胃肠病学 | 2015年 / 20卷 / 11期

关键词：

自噬; 炎症性肠病; Crohn病; 结肠炎,溃疡性; 发病机制; 全基因组关联研究;

D O I：

暂无

中图分类号：

R574 [肠疾病];

学科分类号：

100201 [内科学];

摘要：

炎症性肠病(IBD)是一种慢性、非特异性肠道炎性疾病,其发病机制与环境、遗传以及免疫等多种因素相关。自噬在细胞稳态和机体免疫中发挥重要作用,自噬异常可能参与IBD的发病。全基因组关联分析(GWAS)研究证实,ATG16L1、IRGM、NOD2等自噬相关基因与IBD密切相关。本文就自噬异常在IBD发病机制中的作用作一综述。

引用

页码：683 / 686

页数：4

共 14 条

[1]

An alteration in ATG16L1 stability in Crohn disease [J].

Lassen, Kara G. ;

Xavier, Ramnik J. .

AUTOPHAGY, 2014, 10 (10) :1858-1860

[2]

Association of IL23R and ATG16L1 with susceptibility of Crohn’s disease in Chinese population.[J].Jie Zhang;Jiebin Chen;Jianjun Gu;Huimin Guo;Weichang Chen.Scandinavian Journal of Gastroenterology.2014, 10

[3]

Crohn's Disease-Associated Adherent Invasive Escherichia coli Modulate Levels of microRNAs in Intestinal Epithelial Cells to Reduce Autophagy [J].

Hang Thi Thu Nguyen ;

Dalmasso, Guillaume ;

Mueller, Stefan ;

Carriere, Jessica ;

Seibold, Frank ;

Darfeuille-Michaud, Arlette .

GASTROENTEROLOGY, 2014, 146 (02) :508-519

[4]

MIR106B and MIR93 Prevent Removal of Bacteria From Epithelial Cells by Disrupting ATG16L1-Mediated Autophagy [J].

Lu, Changming ;

Chen, Jianfeng ;

Xu, Hua-Guo ;

Zhou, Xianzheng ;

He, Qiongqiong ;

Li, Yu-Lin ;

Jiang, Guoqing ;

Shan, Yuxi ;

Xue, Boxin ;

Zhao, Rui-Xun ;

Wang, Yong ;

Werle, Kaitlin D. ;

Cui, Rutao ;

Liang, Jiyong ;

Xu, Zhi-Xiang .

GASTROENTEROLOGY, 2014, 146 (01) :188-199

[5]

Associations between PTPN2 polymorphisms and susceptibility to ulcerative colitis and Crohn's disease: a meta-analysis [J].

Zhang, Ji-Xiang ;

He, Jian-Hua ;

Wang, Jun ;

Song, Jia ;

Lei, Hong-Bo ;

Wang, Jing ;

Dong, Wei-Guo .

INFLAMMATION RESEARCH, 2014, 63 (01) :71-79

[6]

Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation [J].

Liu, Bo ;

Gulati, Ajay S. ;

Cantillana, Viviana ;

Henry, Stanley C. ;

Schmidt, Elyse A. ;

Daniell, Xiaoju ;

Grossniklaus, Emily ;

Schoenborn, Alexi A. ;

Sartor, R. Balfour ;

Taylor, Gregory A. .

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2013, 305 (08) :G573-G584

[7]

The Protein ATG16L1 Suppresses Inflammatory Cytokines Induced by the Intracellular Sensors Nod1 and Nod2 in an Autophagy-Independent Manner [J].

Sorbara, Matthew T. ;

Ellison, Lisa K. ;

Ramjeet, Mahendrasingh ;

Travassos, Leonardo H. ;

Jones, Nicola L. ;

Girardin, Stephen E. ;

Philpott, Dana J. .

IMMUNITY, 2013, 39 (05) :858-873

[8]

Atg16L1 deficiency confers protection from uropathogenic Escherichia coli infection in vivo [J].

Wang, Caihong ;

Mendonsa, Graziella R. ;

Symington, Jane W. ;

Zhang, Qunyuan ;

Cadwell, Ken ;

Virgin, Herbert W. ;

Mysorekar, Indira U. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2012, 109 (27) :11008-11013

[9]

Nondegradative Role of Atg5-Atg12/Atg16L1 Autophagy Protein Complex in Antiviral Activity of Interferon Gamma [J].

Hwang, Seungmin ;

Maloney, Nicole S. ;

Bruinsma, Monique W. ;

Goel, Gautam ;

Duan, Erning ;

Zhang, Lei ;

Shrestha, Bimmi ;

Diamond, Michael S. ;

Dani, Adish ;

Sosnovtsev, Stanislav V. ;

Green, Kim Y. ;

Lopez-Otin, Carlos ;

Xavier, Ramnik J. ;

Thackray, Larissa B. ;

Virgin, Herbert W. .

CELL HOST & MICROBE, 2012, 11 (04) :397-409

[10]

Crohn's disease-associated polymorphism within the PTPN2 gene affects muramyl-dipeptide-induced cytokine secretion and autophagy [J].

Scharl, Michael ;

Mwinyi, Jessica ;

Fischbeck, Anne ;

Leucht, Katharina ;

Eloranta, Jyrki J. ;

Arikkat, Joba ;

Pesch, Theresa ;

Kellermeier, Silvia ;

Mair, Alma ;

Kullak-Ublick, Gerd A. ;

Truninger, Kaspar ;

Noreen, Faiza ;

Regula, Jaroslaw ;

Gaj, Pawel ;

Pittet, Valerie ;

Mueller, Christoph ;

Hofmann, Claudia ;

Fried, Michael ;

McCole, Declan F. ;

Rogler, Gerhard .

INFLAMMATORY BOWEL DISEASES, 2012, 18 (05) :900-912

← 1 2 →