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炎症诱导的胃肠道平滑肌“离子通道病”

Inflammation-induced "channelopathies" in the gastrointestinal smooth muscle.

作者信息

Malykhina Anna P, Akbarali Hamid I

机构信息

Department of Physiology, University of Oklahoma, Health Sciences Center, Oklahoma City, OK 73104, USA.

出版信息

Cell Biochem Biophys. 2004;41(2):319-30. doi: 10.1385/CBB:41:2:319.

Abstract

Inflammation markedly alters the motility patterns of the gastrointestinal tract, resulting mostly in decreased excitability of smooth muscle. There is emerging evidence indicating that inflammation alters ion channel expression and function of smooth muscle cells. In this review we summarize studies defining the mechanisms affecting contractile and electrical activity of gastrointestinal smooth muscle. We have focused on the evidence for decreased calcium channel conductance and alterations in the intracellular signaling mechanisms and discuss the role of muscarinic receptor activation in models of gastrointestinal inflammation. We propose that some of the clinical symptoms of altered smooth muscle contraction in pathogenesis of gut disorders such as inflammatory bowel disease may be regulated at the level of the ion channel.

摘要

炎症显著改变胃肠道的运动模式,主要导致平滑肌兴奋性降低。越来越多的证据表明,炎症会改变平滑肌细胞的离子通道表达和功能。在这篇综述中,我们总结了有关影响胃肠道平滑肌收缩和电活动机制的研究。我们重点关注钙通道电导降低的证据以及细胞内信号传导机制的改变,并讨论毒蕈碱受体激活在胃肠道炎症模型中的作用。我们提出,在肠道疾病(如炎症性肠病)发病机制中平滑肌收缩改变的一些临床症状可能在离子通道水平受到调节。

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