Mechanisms of smooth muscle responses to inflammation

被引:53
作者
Shea-Donohue, T. [1 ]
Notari, L.
Sun, R.
Zhao, A.
机构
[1] Univ Maryland, Sch Med, Mucosal Biol Res Ctr, HSFII, Baltimore, MD 21201 USA
基金
美国国家卫生研究院;
关键词
macrophages; myosin light chain kinase; smooth muscle; T-helper cells; TNBS-INDUCED COLITIS; ENDOGENOUS IGF-I; NIPPOSTRONGYLUS-BRASILIENSIS; DOWN-REGULATION; CROHNS-DISEASE; BOWEL-DISEASE; CYTOKINE MODULATION; ULCERATIVE-COLITIS; IMMUNE-MECHANISMS; RNA-INTERFERENCE;
D O I
10.1111/j.1365-2982.2012.01986.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background 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. Purpose 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.
引用
收藏
页码:802 / 811
页数:10
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