Impact of Paneth Cell Autophagy on Inflammatory Bowel Disease.
Impact of Paneth Cell Autophagy on Inflammatory Bowel Disease.
复制标题
潘氏细胞自噬对炎症性肠病的影响。
DOI：
10.3389/fimmu.2018.00693
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发表时间：
2018
影响因子：
7.3
通讯作者：
Bai Y
中科院分区：
文献类型：
--
作者：
Wang SL;Shao BZ;Zhao SB;Fang J;Gu L;Miao CY;Li ZS;Bai Y
肠粘膜屏障主要由黏液层和上皮组成，具有吸收营养和防止病原微生物入侵的功能。Paneth细胞是粘膜屏障的重要组成部分，通过产生抗菌物质和控制宿主-共生平衡，在维持肠道稳态中起着至关重要的作用。目前的证据表明，肠粘膜屏障功能障碍，特别是Paneth细胞功能障碍参与了炎症性肠病（IBD）的发生和发展。自噬是一种细胞应激反应，涉及多种生理过程，如蛋白质的分泌、抗菌肽的产生以及异常细胞器或蛋白质的降解。近年来，自噬在IBD发病机制中的作用得到了越来越多的研究。在本文中，我们主要介绍Paneth细胞自噬在IBD中的作用，以及几种常见的Penath细胞自噬相关基因变异和IBD的相关治疗策略。
Intestinal mucosal barrier, mainly consisting of the mucus layer and epithelium, functions in absorbing nutrition as well as prevention of the invasion of pathogenic microorganisms. Paneth cell, an important component of mucosal barrier, plays a vital role in maintaining the intestinal homeostasis by producing antimicrobial materials and controlling the host-commensal balance. Current evidence shows that the dysfunction of intestinal mucosal barrier, especially Paneth cell, participates in the onset and progression of inflammatory bowel disease (IBD). Autophagy, a cellular stress response, involves various physiological processes, such as secretion of proteins, production of antimicrobial peptides, and degradation of aberrant organelles or proteins. In the recent years, the roles of autophagy in the pathogenesis of IBD have been increasingly studied. Here in this review, we mainly focus on describing the roles of Paneth cell autophagy in IBD as well as several popular autophagy-related genetic variants in Penath cell and the related therapeutic strategies against IBD.
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影响因子：
30.3
作者：
Burger E;Araujo A;López-Yglesias A;Rajala MW;Geng L;Levine B;Hooper LV;Burstein E;Yarovinsky F
通讯作者：
Yarovinsky F
影响因子：
13.3
作者：
Cabrera, Sandra;Fernandez, Alvaro F.;Lopez-Otin, Carlos
通讯作者：
Lopez-Otin, Carlos
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
4.9
作者：
Ananthakrishnan, Ashwin N.;McGinley, Emily L.;Saeian, Kia
通讯作者：
Saeian, Kia
影响因子：
64.5
作者：
Cadwell K;Patel KK;Maloney NS;Liu TC;Ng AC;Storer CE;Head RD;Xavier R;Stappenbeck TS;Virgin HW
通讯作者：
Virgin HW