Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium

被引：127

作者：

Nunes, Tiago ^{[1
]}

Bernardazzi, Claudio ^{[2
,3
]}

de Souza, Heitor S. ^{[2
,3
,4
]}

机构：

[1] Tech Univ Munich, ZIEL Res Ctr Nutr & Food Sci, Nutr & Immunol Chair, D-85354 Freising Weihenstephan, Germany

[2] Univ Fed Rio de Janeiro, Univ Hosp, Serv Gastroenterol, BR-21941913 Rio De Janeiro, RJ, Brazil

[3] Univ Fed Rio de Janeiro, Univ Hosp, Lab Multidisciplinar Pesquisa, BR-21941913 Rio De Janeiro, RJ, Brazil

[4] DOr Inst Res & Educ IDOR, BR-22281100 Rio De Janeiro, RJ, Brazil

来源：

BIOMED RESEARCH INTERNATIONAL | 2014年 / 2014卷

关键词：

ILEAL CROHNS-DISEASE; MUCOSAL T-CELLS; ULCERATIVE-COLITIS; GENE ATG16L1; MOLECULAR-MECHANISMS; STEM-CELLS; IRGM; SUSCEPTIBILITY; EXPRESSION; PROTEIN;

D O I：

10.1155/2014/218493

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Cell death mechanisms have been associated with the development of inflammatory bowel diseases in humans and mice. Recent studies suggested that a complex crosstalk between autophagy/apoptosis, microbe sensing, and enhanced endoplasmic reticulum stress in the epithelium could play a critical role in these diseases. In addition, necroptosis, a relatively novel programmed necrosis like pathway associated with TNF receptor activation, seems to be also present in the pathogenesis of Crohn's disease and in specific animal models for intestinal inflammation. This review attempts to cover new data related to cell death mechanisms and inflammatory bowel diseases.

引用

页数：12

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