From the Department of Surgery (D.C., E.L., J.L., S.A., S.L., K.R., B.L.), University of Michigan, Ann Arbor, Michigan; and Regenerative Medicine Department (A.T.Q., T.A.D.), Naval Medical Research Center, Silver Spring, Maryland.
J Trauma Acute Care Surg. 2017 Jan;82(1):174-184. doi: 10.1097/TA.0000000000001290.
Muscle fibrosis, the disruption, of functional parenchyma by stromal elements, is an often overlooked sequela of traumatic muscle injury, ageing, and congenital disease. The remarkable regenerative capacity of skeletal muscle is dependent on the interaction of myogenic progenitors and the same stromal connective tissue elements responsible for fibrosis generation and propagation. The coordination of effective therapeutic strategies to mitigate muscle fibrosis following injury requires a clear understanding of the prominent cellular progenitors, extracellular constituents, and signaling mechanisms involved in muscle healing. Recent studies have begun to elucidate the critical cellular processes that delineate physiologic regeneration and dysregulated healing resulting in muscle fibrosis. This review presents the salience of these novel findings in the context of the current treatment paradigms for muscle fibrosis.
肌肉纤维化是指基质成分对功能性实质组织的破坏,是外伤性肌肉损伤、衰老和先天性疾病的常见后遗症。骨骼肌具有显著的再生能力,这依赖于成肌祖细胞与间质结缔组织成分之间的相互作用,而后者是导致纤维化产生和发展的关键因素。为了在损伤后减轻肌肉纤维化,需要制定有效的治疗策略,这就要求我们清楚地了解肌肉愈合过程中涉及的主要细胞祖代、细胞外成分和信号机制。最近的研究已经开始阐明这些新发现对阐明生理再生和失调愈合导致肌肉纤维化的关键细胞过程的重要意义。本文综述了这些新发现对当前肌肉纤维化治疗模式的重要意义。