Mucosal Biology Research Center and Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Neurogastroenterol Motil. 2012 Sep;24(9):802-11. doi: 10.1111/j.1365-2982.2012.01986.x.
Inflammation-induced changes in smooth muscle may be the consequence of changes in the properties of smooth muscle itself, in the control by nerves and hormones, in the microenvironment, or in the balance of constitutive or induced mediators. A general concept is that the specific characteristics and effects of inflammation can be linked to the nature of the infiltrate and the associated mediators, which are dictated predominantly by the immune environment. Inflammatory mediators may regulate smooth muscle function by directly acting on smooth muscle cells or, indirectly, through stimulation of the release of mediators from other cells. In addition, smooth muscle is not a passive bystander during inflammation and our knowledge of molecular signaling pathways that control smooth muscle function, and the contribution of the immune mechanisms to smooth muscle homeostasis, has expanded greatly in the last decade. Recent studies also demonstrated the relevance of extracellular proteases, of endogenous or exogenous origin, redox imbalance, or epigenetic mechanisms, to gastrointestinal dismotility and inflammation in the context of functional and organic disorders.
In this review we discuss the various types of inflammation and the established and emerging mechansims of inflammation-induced changes in smooth muscle morphology and function.
炎症引起的平滑肌变化可能是平滑肌本身特性变化、神经和激素控制变化、微环境变化或固有或诱导介质平衡变化的结果。一个普遍的概念是，炎症的特定特征和影响可以与浸润的性质和相关的介质联系起来，这些介质主要由免疫环境决定。炎症介质可以通过直接作用于平滑肌细胞或间接通过刺激其他细胞释放介质来调节平滑肌功能。此外，在炎症过程中，平滑肌并不是一个被动的旁观者，在过去十年中，我们对控制平滑肌功能的分子信号通路以及免疫机制对平滑肌稳态的贡献有了很大的了解。最近的研究还表明，细胞外蛋白酶（内源性或外源性来源）、氧化还原失衡或表观遗传机制与功能和器质性障碍中胃肠道动力障碍和炎症有关。
在这篇综述中，我们讨论了各种类型的炎症以及炎症引起的平滑肌形态和功能变化的既定和新兴机制。
