Lin Fu, Sun Liankun, Zhang Yu, Gao Weinan, Chen Zihan, Liu Yanan, Tian Kai, Han Xuyu, Liu Ruize, Li Yang, Shen Luyan
Key Laboratory of Pathobiology, Department of Pathophysiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, China.
Experimental Teaching Center of Basic Medicine, College of Basic Medical Sciences, Jilin University, Changchun, China.
Front Cell Dev Biol. 2024 Apr 12;12:1381417. doi: 10.3389/fcell.2024.1381417. eCollection 2024.
Regeneration and repair are prerequisites for maintaining effective function of skeletal muscle under high energy demands, and myogenic differentiation is one of the key steps in the regeneration and repair process. A striking feature of the process of myogenic differentiation is the alteration of mitochondria in number and function. Mitochondrial dysfunction can activate a number of transcriptional, translational and post-translational programmes and pathways to maintain cellular homeostasis under different types and degrees of stress, either through its own signaling or through constant signaling interactions with the nucleus and cytoplasm, a process known as the mitochondrial stress responses (MSRs). It is now believed that mitochondrial dysfunction is closely associated with a variety of muscle diseases caused by reduced levels of myogenic differentiation, suggesting the possibility that MSRs are involved in messaging during myogenic differentiation. Also, MSRs may be involved in myogenesis by promoting bioenergetic remodeling and assisting myoblast survival during myogenic differentiation. In this review, we will take MSRs as an entry point to explore its concrete regulatory mechanisms during myogenic differentiation, with a perspective to provide a theoretical basis for the treatment and repair of related muscle diseases.
再生和修复是在高能量需求下维持骨骼肌有效功能的先决条件,而成肌分化是再生和修复过程中的关键步骤之一。成肌分化过程的一个显著特征是线粒体在数量和功能上的改变。线粒体功能障碍可通过自身信号传导或通过与细胞核和细胞质的持续信号相互作用,激活许多转录、翻译和翻译后程序及途径,以在不同类型和程度的应激下维持细胞稳态,这一过程称为线粒体应激反应(MSRs)。现在人们认为,线粒体功能障碍与多种因成肌分化水平降低引起的肌肉疾病密切相关,这表明MSRs可能参与成肌分化过程中的信号传递。此外,MSRs可能通过促进生物能量重塑和在成肌分化过程中协助成肌细胞存活而参与肌生成。在这篇综述中,我们将以MSRs为切入点,探讨其在成肌分化过程中的具体调控机制,以期为相关肌肉疾病的治疗和修复提供理论依据。