Aberrant repair and fibrosis development in skeletal muscle.
Aberrant repair and fibrosis development in skeletal muscle.
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DOI：
10.1186/2044-5040-1-21
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发表时间：
2011-05-04
期刊：
影响因子：
4.9
通讯作者：
Muñoz-Cánoves P
中科院分区：
文献类型：
--
作者：
Mann CJ;Perdiguero E;Kharraz Y;Aguilar S;Pessina P;Serrano AL;Muñoz-Cánoves P
受损组织的修复过程涉及多种细胞类型响应局部和全身信号的协调活动。急性组织损伤后，浸润的炎症细胞和驻留干细胞协调其活动以恢复组织稳态。然而，在慢性组织损伤期间，例如肌营养不良症，炎症细胞浸润和成纤维细胞活化持续存在，而干细胞（卫星细胞）的修复能力却减弱。异常的营养不良性肌肉修复及其末期纤维化代表了几乎所有慢性神经退行性肌肉疾病的最终共同途径。随着我们对肌肉纤维化发病机制的了解不断深入，很明显，肌肉为局部微环境调节组织修复提供了有用的模型，显示了哺乳动物伤口愈合反应的肌肉特异性干细胞、炎症细胞、成纤维细胞和细胞外基质成分之间的相互作用。本文回顾了正常与异常肌肉组织修复机制的最新发现。
The repair process of damaged tissue involves the coordinated activities of several cell types in response to local and systemic signals. Following acute tissue injury, infiltrating inflammatory cells and resident stem cells orchestrate their activities to restore tissue homeostasis. However, during chronic tissue damage, such as in muscular dystrophies, the inflammatory-cell infiltration and fibroblast activation persists, while the reparative capacity of stem cells (satellite cells) is attenuated. Abnormal dystrophic muscle repair and its end stage, fibrosis, represent the final common pathway of virtually all chronic neurodegenerative muscular diseases. As our understanding of the pathogenesis of muscle fibrosis has progressed, it has become evident that the muscle provides a useful model for the regulation of tissue repair by the local microenvironment, showing interplay among muscle-specific stem cells, inflammatory cells, fibroblasts and extracellular matrix components of the mammalian wound-healing response. This article reviews the emerging findings of the mechanisms that underlie normal versus aberrant muscle-tissue repair.
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