Alway Stephen E, Paez Hector G, Pitzer Christopher R
Laboratory of Muscle Biology and Sarcopenia, Department of Physical Therapy, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Department of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Muscles. 2023 Mar 24;2(2):119-163. doi: 10.3390/muscles2020011.
Musculoskeletal health is directly linked to independence and longevity, but disease and aging impairs muscle mass and health. Complete repair after a pathological or physiological muscle injury is critical for maintaining muscle function, yet muscle repair is compromised after disuse, or in conditions such as metabolic diseases, cancer, and aging. Regeneration of damaged tissue is critically dependent upon achieving the optimal function of satellite cells (muscle stem cells, MSCs). MSC remodeling in muscle repair is highly dependent upon its microenvironment, and metabolic health of MSCs, which is dependent on the functional capacity of their mitochondria. Muscle repair is energy demanding and mitochondria provide the primary source for energy production during regeneration. However, disease and aging induce mitochondrial dysfunction, which limits energy production during muscle regeneration. Nevertheless, the role of mitochondria in muscle repair likely extends beyond the production of ATP and mitochondria could provide potentially important regulatory signaling to MSCs during repair from injury. The scope of current research in muscle regeneration extends from molecules to exosomes, largely with the goal of understanding ways to improve MSC function. This review focuses on the role of mitochondria in skeletal muscle myogenesis/regeneration and repair. A therapeutic strategy for improving muscle mitochondrial number and health will be discussed as a means for enhancing muscle regeneration. Highlights: (a). Mitochondrial dysfunction limits muscle regeneration; (b). Muscle stem cell (MSC) function can be modulated by mitochondria; (c). Enhancing mitochondria in MSCs may provide a strategy for improving muscle regeneration after an injury.
肌肉骨骼健康与独立性和长寿直接相关，但疾病和衰老会损害肌肉质量和健康。病理性或生理性肌肉损伤后的完全修复对于维持肌肉功能至关重要，然而，在废用状态下，或在代谢疾病、癌症和衰老等情况下，肌肉修复会受到损害。受损组织的再生严重依赖于卫星细胞（肌肉干细胞，MSCs）实现最佳功能。肌肉修复过程中MSCs的重塑高度依赖于其微环境以及MSCs的代谢健康，而这又取决于其线粒体的功能能力。肌肉修复需要能量，线粒体是再生过程中能量产生的主要来源。然而，疾病和衰老会诱导线粒体功能障碍，从而限制肌肉再生过程中的能量产生。尽管如此，线粒体在肌肉修复中的作用可能不仅限于ATP的产生，线粒体在损伤修复过程中可能会向MSCs提供潜在重要的调节信号。目前肌肉再生研究的范围从分子到外泌体，主要目标是了解改善MSCs功能的方法。本综述重点关注线粒体在骨骼肌生成/再生和修复中的作用。将讨论一种改善肌肉线粒体数量和健康的治疗策略，作为增强肌肉再生的一种手段。要点：（a）线粒体功能障碍限制肌肉再生；（b）线粒体可调节肌肉干细胞（MSC）的功能；（c）增强MSCs中的线粒体可能为改善损伤后肌肉再生提供一种策略。
