Center for Genetic Muscle Disorders, The Kennedy Krieger Institute, The Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Curr Opin Rheumatol. 2011 Nov;23(6):568-73. doi: 10.1097/BOR.0b013e32834bac92.
This review evaluates recently published literature examining various muscle tissue cells and their modulators that determine whether injured skeletal muscle will fully regenerate or become fibrotic.
Muscle regeneration is a complex process involving several interacting cell types. Macrophages initiate a cytokine response to injury that both directs the subsequent inflammatory response and promotes nonmyeloid proliferation. Muscle cells and their progenitors produce autocrine and paracrine growth factors that help inhibit or stimulate muscle growth and regeneration. Cells of the connective tissue, including fibroblasts and newly described fibro/adipogenic progenitors, can support myogenic cells and remodel the extracellular matrix. However in certain environments, fibrosis can become a self-perpetuating process leading to incomplete muscle regeneration.
Several cell types are involved in the muscle repair process, interacting through multiple signaling molecules and pathways. This provides a richness of potential therapeutic targets to reduce fibrosis and facilitate skeletal muscle regeneration.
本篇综述评估了近期发表的文献，这些文献研究了各种肌肉组织细胞及其调节剂，以确定受伤的骨骼肌是完全再生还是纤维化。
肌肉再生是一个复杂的过程，涉及几种相互作用的细胞类型。巨噬细胞启动细胞因子反应以应对损伤，这既指导随后的炎症反应，又促进非髓细胞增殖。肌肉细胞及其祖细胞产生自分泌和旁分泌生长因子，有助于抑制或刺激肌肉生长和再生。结缔组织细胞，包括成纤维细胞和新描述的成纤维/脂肪祖细胞，可以支持肌细胞并重塑细胞外基质。然而，在某些环境中，纤维化可能成为一个自我维持的过程，导致肌肉再生不完全。
几种细胞类型参与肌肉修复过程，通过多种信号分子和途径相互作用。这为减少纤维化和促进骨骼肌再生提供了丰富的潜在治疗靶点。
