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Journal of Zhejiang University SCIENCE B
ISSN 1673-1581(Print), 1862-1783(Online), Monthly
2016 Vol.17 No.1 P.1-9
Nerve growth factor and diarrhea-predominant irritable bowel syndrome (IBS-D): a potential therapeutic target?
Abstract: Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized by recurrent abdominal pain or discomfort associated with abnormal bowel habits. Diarrhea-predominant IBS (IBS-D) is a major subtype of IBS, the predominant manifestations of which are abdominal pain and diarrhea. The pathogenesis of IBS-D remained unknown until recently. The effects of psychosocial stress, central hypervigilance, neuroendocrine abnormality, disturbed gastrointestinal motility, mucosal immune activation, intestinal barrier dysfunction, visceral hypersensitivity (VH), altered gut flora, and genetic susceptibility may be involved in its development. Recently, increased attention has been placed on the neural-immune-endocrine network mechanism in IBS-D, especially the role of various neuroendocrine mediators. As a member of the neurotrophin family, nerve growth factor (NGF) has diverse biological effects, and participates in the pathogenesis of many diseases. Basic studies have demonstrated that NGF is associated with inflammatory- and stress-related VH, as well as stress-related intestinal barrier dysfunction. The aim of this study is to summarize recent literature and discuss the role of NGF in the pathophysiology of IBS-D, especially in VH and intestinal barrier dysfunction, as well as its potential as a therapeutic target in IBS-D.
Key words: Nerve growth factor, Diarrhea-predominant irritable bowel syndrome, Pathophysiology, Intestinal barrier dysfunction, Visceral hypersensitivity
创新点:总结了国内外有关NGF参与IBS-D病理生理学的基础及临床研究证据,提出了NGF介导IBS-D内脏高敏感和肠屏障功能受损的可能机制,并首次构建了NGF-肥大细胞-神经纤维三者在IBS-D发病中的作用网络。
方法:在PubMed、EMBASE、Web of Science、CNKI、维普和万方等数据库检索有关NGF参与IBS-D病理生理学的中英文文献,时间设定为各数据库建库至2015年5月。剔除重复及不相关文献后,对纳入文献进行综述。
结论:NGF作为重要的神经内分泌介质,可能参与介 导了IBS-D患者内脏高敏感和肠屏障功能受损,其在IBS-D病理生理学中的作用值得深入研究,并有望成为治疗靶点。
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Open peer comments: Debate/Discuss/Question/Opinion
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DOI:
10.1631/jzus.B1500181
CLC number:
R574.4
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On-line Access:
2024-08-27
Received:
2023-10-17
Revision Accepted:
2024-05-08
Crosschecked:
2015-12-16