期刊
EXPERIMENTAL AND THERAPEUTIC MEDICINE
卷 13, 期 4, 页码 1187-1193出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2017.4133
关键词
irritable bowel syndrome; gastrointestinal motility; stem cell factor (SCF); c-Kit; ligand; receptor tyrosine kinase signaling system; inflammation; neuromodulation
资金
- Guangdong province Nature Science Foundation of China [2014A030313404]
- Natural Science Foundation of China [81673842]
- 'Excellent Doctoral Dissertation Incubation Grant' from the First Clinical School of Guangzhou University of Chinese Medicine [YB201402]
Irritable bowel syndrome (IBS) is a functional bowel disease with a complicated etiopathogenesis, often characterized by gastrointestinal motility disorder and high visceral sensitivity. IBS is a comprehensive multi-systemic disorder, with the interaction of multiple factors, such as mental stress, intestinal function and flora, heredity, resulting in the disease. The existence of a common mechanism underlying the aforementioned factors is currently unknown. The lack of therapies that comprehensively address the disease symptoms, including abdominal pain and diarrhea, is a limitation of current IBS management. The current review has explored the role of the SCF/c-Kit receptor/ligand system in IBS. The SCF/c-Kit system constitutes a classical ligand/receptor tyrosine kinase signaling system that mediates inflammation and smooth muscle contraction. Additionally, it provides trophic support to neural crest-derived cell types, including the enteric nervous system and mast cells. The regulation of SCF/c-Kit on the interstitial cells of Cajal (ICC) suggest that it may play a key role in the aberrant intestinal dynamics and high visceral sensitivity observed in IBS. The role of the SCF/c-Kit system in intestinal motility, inflammation and nerve growth has been reported. From the available biomedical evidence on the pathogenesis of IBS, it has been concluded that the SCF-c-Kit system is a potential therapeutic target for rational drug design in the treatment of IBS.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据