Department of Experimental and Health Sciences, Cell Biology Unit, CIBERNED, Pompeu Fabra University, Barcelona, Spain.
Curr Top Dev Biol. 2011;96:167-201. doi: 10.1016/B978-0-12-385940-2.00007-3.
The repair of an injured tissue is a complex biological process involving the coordinated activities of tissue-resident and infiltrating cells in response to local and systemic signals. Following acute tissue injury, inflammatory cell infiltration and activation/proliferation of resident stem cells is the first line of defense to restore tissue homeostasis. However, in the setting of chronic tissue damage, such as in Duchenne Muscular Dystrophy, inflammatory infiltrates persist, the ability of stem cells (satellite cells) is blocked and fibrogenic cells are continuously activated, eventually leading to the conversion of muscle into nonfunctional fibrotic tissue. This review explores our current understanding of the cellular and molecular mechanisms underlying efficient muscle repair that are dysregulated in muscular dystrophy-associated fibrosis and in aging-related muscle dysfunction.
组织损伤的修复是一个复杂的生物学过程，涉及组织驻留细胞和浸润细胞对局部和全身信号的协调活动。在急性组织损伤后，炎症细胞浸润和驻留干细胞的激活/增殖是恢复组织内稳态的第一道防线。然而，在慢性组织损伤的情况下，如在杜氏肌营养不良症中，炎症浸润持续存在，干细胞（卫星细胞）的能力被阻断，纤维生成细胞持续被激活，最终导致肌肉转化为无功能的纤维组织。本综述探讨了我们目前对肌肉修复的细胞和分子机制的理解，这些机制在与肌肉营养不良相关的纤维化和与年龄相关的肌肉功能障碍中失调。
