Pathophysiology of Volumetric Muscle Loss Injury

Pathophysiology of Volumetric Muscle Loss Injury
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DOI:
10.1159/000443925
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发表时间:
2015-01-01
影响因子:
2.7
通讯作者:
Ward, Catherine L.
Ward, Catherine L.
中科院分区:
生物学4区
文献类型:
--
作者:
Corona, Benjamin T.;Wenke, Joseph C.;Ward, Catherine L.

文献摘要

被引文献

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容积性肌肉丧失(VML)损伤在平民和军事创伤患者中普遍存在,并且已知会造成慢性功能缺陷。定义VML损伤的肌肉组织的坦率损失超出了哺乳动物骨骼肌的强大修复和再生能力。鉴于VML损伤的性质,显然需要开发促进骨骼肌纤维从头再生的疗法,骨骼肌纤维可以与剩余的肌肉组织整合并恢复肌肉力量。然而,VML损伤的病理生理学尚未完全确定,因此,除了从头再生之外,可能还有其他机会改善功能结局。在此,VML的临床和临床前研究进行了审查,以确定VML损伤,可以损害肢体功能和肌肉力量的显着表现。有限的临床数据突出了继发于VML损伤的增生性纤维化作为改善肢体活动度的可行目标。使用标准化神经肌肉功能评估的选定临床前研究广泛地确定,VML损伤后剩余的肌肉质量表现不佳,因此,VML力量缺陷百分比明显比收缩机制最初的坦率损失更差。文献中提出的剩余肌肉质量的次优强度的潜在机制包括肌内神经损伤、肌肉结构扰动和力传递减少。总的来说,临床和临床前数据都表明VML后存在复杂的病理生理学,存在多种治疗靶点。这是美国政府的作品,在美国不受版权保护。外国版权可能适用。由S发布。Karger AG,巴塞尔
Volumetric muscle loss ( VML) injuries are prevalent in civilian and military trauma patients and are known to impart chronic functional deficits. The frank loss of muscle tissue that defines VML injuries is beyond the robust reparative and regenerative capacities of mammalian skeletal muscle. Given the nature of VML injuries, there is a clear need to develop therapies that promote de novo regeneration of skeletal muscle fibers, which can integrate with the remaining musculature and restore muscle strength. However, the pathophysiology of VML injuries is not completely defined, and, therefore, there may be other opportunities to improve functional outcomes other than de novo regeneration. Herein, clinical and preclinical studies of VML were reviewed to ascertain salient manifestations of VML injury that can impair limb function and muscle strength. The limited clinical data available highlighted proliferative fibrosis secondary to VML injury as a viable target to improve limb range of motion. Selected pre-clinical studies that used standardized neuromuscular functional assessments broadly identified that the muscle mass remaining after VML injury is performing suboptimally, and, therefore, percent VML strength deficits are significantly worse than can be explained by the initial frank loss of contractile machinery. Potential mechanisms of suboptimal strength of the remaining muscle mass suggested within the literature include intramuscular nerve damage, muscle architectural perturbations, and diminished transmission of force. Collectively, both clinical and preclinical data indicate a complex pathophysiology after VML that presents multiple therapeutic targets. This is a work of the US Government and is not subject to copyright protection in the USA. Foreign copyrights may apply. Published by S. Karger AG, Basel