Smooth muscle cells (SMC) make up the muscular portion of the gastrointestinal (GI) tract from the distal oesophagus to the internal anal sphincter. Coordinated contractions of these cells produce the motor patterns of GI motility. Considerable progress was made during the last 20 years to understand the basic mechanisms controlling excitation-contraction (E-C) coupling. The smooth muscle motor is now understood in great molecular detail, and much has been learned about the mechanisms that deliver and recover Ca2+ during contractions. The majority of Ca2+ that initiates contractions comes from the external solution and is supplied by voltage-dependent Ca2+ channels (VDCC). VDCC are regulated largely by the effects of K+ and non-selective cation conductances (NSCC) on cell membrane potential and excitability. Ca2+ entry is supplemented by release of Ca2+ from IP(3) receptor-operated stores and by mechanisms that alter the sensitivity of the contractile apparatus to changes in cytoplasmic Ca2+. Molecular studies of the regulation of smooth muscle have been complicated by the plasticity of SMC and difficulties in culturing these cells without dramatic phenotypic changes. Major questions remain to be resolved regarding the details of E-C coupling in human GI smooth muscles. New discoveries regarding molecular expression that give GI smooth muscle their unique properties, the phenotypic changes that occur in SMC in GI motor disorders, tissue engineering approaches to repair or replace defective muscular regions, and molecular manipulations of GI smooth muscles in animals models and in cell culture will be topics for exciting investigations in the future.

译文

平滑肌细胞 (SMC) 构成胃肠道 (GI) 从远端食道到肛门内括约肌的肌肉部分。这些细胞的协调收缩产生胃肠道运动的运动模式。在过去的20年中,在了解控制激发-收缩 (E-C) 耦合的基本机制方面取得了相当大的进展。平滑肌运动现在已经在分子上得到了很大的了解,并且已经了解了在收缩过程中传递和恢复Ca2的机制。引发收缩的大部分Ca2来自外部解决方案,并由电压相关的Ca2通道 (VDCC) 提供。VDCC在很大程度上受K和非选择性阳离子电导 (NSCC) 对细胞膜电位和兴奋性的影响。通过从IP(3) 受体操作的存储中释放Ca2以及通过改变收缩装置对细胞质Ca2变化的敏感性的机制来补充Ca2的进入。平滑肌调节的分子研究因SMC的可塑性和难以培养这些细胞而没有显着的表型变化而变得复杂。关于人类胃肠道平滑肌中E-C耦合的细节,仍有主要问题有待解决。关于赋予GI平滑肌独特特性的分子表达的新发现,在GI运动障碍中SMC中发生的表型变化,修复或替换有缺陷的肌肉区域的组织工程方法,在动物模型和细胞培养中,GI平滑肌的分子操纵将成为未来令人兴奋的研究的主题。

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