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炎症性肠病中肠道运动异常的机制:平滑肌收缩是如何减弱的?

Mechanism of abnormal intestinal motility in inflammatory bowel disease: how smooth muscle contraction is reduced?

作者信息

Ohama Takashi, Hori Masatoshi, Ozaki Hiroshi

机构信息

Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo, Japan.

出版信息

J Smooth Muscle Res. 2007 Apr;43(2):43-54. doi: 10.1540/jsmr.43.43.

Abstract

Intestinal inflammation alters the contractile activity of intestinal smooth muscle. Motility disorders of the gastrointestinal tract are clinically important symptoms, because they are often associated with severe interstitial inflammation. In addition, the motility disorders secondarily induce abnormal growth of the intestinal flora, and the resulting disturbance of this flora aggravates the pathogenesis of mucosal inflammation. This in turn aggravates the intestinal dysmotility; i.e., it is an inflammatory spiral. Therefore, it is important to elucidate the mechanisms involved in the changes in motor function which occur in intestinal inflammation. Recent studies have revealed several molecular mechanisms responsible for the decreased motility which occurs in an inflamed gastrointestinal tract. In the present review, we discuss the functional failure of smooth muscle cells, including changes in the activity of muscarinic receptors, ion channels and the endogenous myosin phosphatase inhibitor CPI-17.

摘要

肠道炎症会改变肠道平滑肌的收缩活动。胃肠道运动障碍是临床上的重要症状,因为它们常与严重的间质炎症相关。此外,运动障碍会继发肠道菌群异常生长,而由此导致的菌群紊乱会加重黏膜炎症的发病机制。这反过来又会加重肠道运动障碍;也就是说,这是一个炎症螺旋。因此,阐明肠道炎症中发生的运动功能变化所涉及的机制很重要。最近的研究揭示了几种导致发炎胃肠道运动性降低的分子机制。在本综述中,我们讨论了平滑肌细胞的功能衰竭,包括毒蕈碱受体、离子通道活性的变化以及内源性肌球蛋白磷酸酶抑制剂CPI-17。

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