Signaling Pathways Associated with Inflammatory Bowel Disease
Signaling Pathways Associated with Inflammatory Bowel Disease
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DOI：
10.2174/187221310791163071
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发表时间：
2010-01-01
影响因子：
4.2
通讯作者：
Feng, Jiexiong
中科院分区：
文献类型：
--
作者：
Wei, Jia;Feng, Jiexiong
炎症性肠病（IBD）包括克罗恩病（CD）和溃疡性结肠炎（UC）。它被认为是由遗传、肠道免疫系统异常免疫反应和肠粘膜抵抗肠道细菌的屏障功能障碍引起的。突变基因可以通过某些信号通路影响 IBD 的发展。异常信号通路在炎症过程中发挥重要作用，可导致炎症反应失调，在 IBD 的发病机制中至关重要。信号通路主要包括P38 MAPK、JNK MAPK、PI3K/Akt、NF-kappa B信号通路。肠道微生物在疾病的发生和维持中发挥着关键作用。 TLR、NF-kappa B 等信号通路的紊乱可作用于肠道屏障，导致效应 T 细胞不受抑制地释放，而效应 T 细胞是介导 CD 炎症的核心细胞。这篇综述重点介绍了相关专利以及对 IBD 相关信号通路的新见解，将有助于开发更好的治疗方法。
Inflammatory bowel disease (IBD) consists of Crohn's disease (CD) and ulcerative colitis (UC). It is thought to be caused by genetic, abnormal immune response of the intestinal immune system and dysfunction of intestinal mucosal barrier against enteric bacteria. Mutational genes can affect the development of IBDs via certain signaling pathways. The abnormal signaling pathways play an important role in the inflammatory process and can lead to dysregulation of the inflammatory response and are crucial in the pathogenesis of IBDs. The signaling pathways mainly include P38 MAPK, JNK MAPK, PI3K/Akt, NF-kappa B signaling pathways. Intestinal microorganisms play a key role in the initiation and maintenance of disease. Disorders of signaling pathways including TLR, NF-kappa B can act on the intestinal barrier, and cause uninhibitedly release of effector T cells which are the central cells mediating inflammation in CD. This review highlights relevant patents and a new insight of signaling pathways associated with IBDs will help to develop better therapeutic approaches.