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膜受体信号转导对慢性内脏痛的贡献。

Contribution of membrane receptor signalling to chronic visceral pain.

机构信息

Illawarra Health & Medical Research Institute (IHMRI), University of Wollongong, Wollongong, NSW, 2522, Australia.

Visceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, SA, 5042, Australia; Centre for Nutrition and Gastrointestinal Diseases, Discipline of Medicine, University of Adelaide, South Australian Health and Medical Research Institute (SAHMRI), North Terrace, Adelaide, SA, 5000, Australia.

出版信息

Int J Biochem Cell Biol. 2018 May;98:10-23. doi: 10.1016/j.biocel.2018.02.017. Epub 2018 Mar 21.

Abstract

Irritable bowel syndrome and inflammatory bowel disease are major forms of chronic visceral pain, which affect over 15% of the global population. In order to identify new therapies, it is important to understand the underlying causes of chronic visceral pain. This review provides recent evidence demonstrating that inflammation or infection of the gastrointestinal tract triggers specific changes in the neuronal excitability of sensory pathways responsible for the transmission of nociceptive information from the periphery to the central nervous system. Specific changes in the expression and function of a variety of ion channels and receptors have been documented in inflammatory and chronic visceral pain conditions relevant to irritable bowel syndrome and inflammatory bowel disease. An increase in pro-nociceptive mechanisms enhances peripheral drive from the viscera and provides an underlying basis for enhanced nociceptive signalling during chronic visceral pain states. Recent evidence also highlights increases in anti-nociceptive mechanisms in models of chronic visceral pain, which present novel targets for pharmacological treatment of this condition.

摘要

肠易激综合征和炎症性肠病是慢性内脏痛的主要形式,影响全球超过 15%的人口。为了确定新的治疗方法,了解慢性内脏痛的根本原因很重要。这篇综述提供了最近的证据,表明胃肠道的炎症或感染会引发感觉通路神经元兴奋性的特定变化,这些通路负责将伤害性信息从外周传递到中枢神经系统。在与肠易激综合征和炎症性肠病相关的炎症性和慢性内脏痛情况下,已经记录了多种离子通道和受体的表达和功能的特定变化。促伤害性机制的增加增强了来自内脏的外周驱动力,并为慢性内脏痛状态下增强的伤害性信号提供了潜在基础。最近的证据还强调了慢性内脏痛模型中抗伤害性机制的增加,这为这种疾病的药物治疗提供了新的靶点。

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