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纤维化和胃肠道炎症的主题。

Themes in fibrosis and gastrointestinal inflammation.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2011 May;300(5):G677-83. doi: 10.1152/ajpgi.00104.2011. Epub 2011 Mar 17.

DOI:10.1152/ajpgi.00104.2011
PMID:21415411
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3094134/
Abstract

Wound healing is an appropriate response to inflammation and tissue injury in the gastrointestinal tract. If wound healing responses are excessive, perpetuated, or prolonged, they lead to fibrosis, distortion of tissue architecture, and loss of function. This introductory editorial and the minireviews or reviews in this themes series highlight the diversity in severity and location of fibrosis in response to gastrointestinal inflammation. The multiplicity of cellular and molecular mediators and new players, including stem cells or extracellular matrix-producing cells derived from nonmesenchymal cell types, is reviewed. Comparisons of inflammation-induced fibrosis across organ systems and the need for integrated and systems-based molecular approaches, new imaging modalities, well-characterized animal models, cell culture models, and improved diagnostic or predictive markers are reviewed. To date, intestinal fibrosis has received much less attention than inflammation in terms of defining mechanisms and underlying causes. This themes series aims to illustrate the importance of research in this area in gastrointestinal health and disease.

摘要

创伤愈合是胃肠道炎症和组织损伤的适当反应。如果创伤愈合反应过度、持续或延长,就会导致纤维化、组织结构变形和功能丧失。本引言社论和本专题系列中的小型评论或综述强调了纤维化在胃肠道炎症中的严重程度和位置的多样性。本文回顾了多种细胞和分子介质以及新的参与者,包括源自非间充质细胞类型的干细胞或产生细胞外基质的细胞。还回顾了跨器官系统诱导炎症性纤维化的比较,以及对综合和基于系统的分子方法、新的成像方式、特征明确的动物模型、细胞培养模型和改进的诊断或预测标志物的需求。到目前为止,与炎症相比,肠道纤维化在定义机制和潜在原因方面受到的关注要少得多。本专题系列旨在说明该领域研究在胃肠道健康和疾病中的重要性。

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本文引用的文献

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Maternal obesity induces sustained inflammation in both fetal and offspring large intestine of sheep.母体肥胖会导致绵羊胎儿和后代的大肠持续发炎。
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Epigenetic histone methylation modulates fibrotic gene expression.表观遗传组蛋白甲基化调节纤维化基因表达。
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High-fat diet: bacteria interactions promote intestinal inflammation which precedes and correlates with obesity and insulin resistance in mouse.高脂饮食:细菌相互作用促进肠道炎症,这种炎症先于肥胖和胰岛素抵抗发生,并与肥胖和胰岛素抵抗相关。
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