期刊
FEBS JOURNAL
卷 289, 期 21, 页码 6463-6483出版社
WILEY
DOI: 10.1111/febs.16372
关键词
cytokine; myogenesis; myogenic differentiation; regeneration; skeletal muscle
资金
- National Institute of Health (NIAMS) [AR048914]
- National Institute of Health (NIGMS) [GM089771]
Regeneration of adult skeletal muscle in mammals is a complex process regulated by multiple proteins and signaling pathways. Cytokines play a crucial role in skeletal myogenesis, with both infiltrating immune cells and the muscle itself secreting these signaling molecules. This review focuses on muscle-secreted cytokines that have been shown to be involved in myogenic differentiation and muscle regeneration.
Regeneration of the mammalian adult skeletal muscle is a well-orchestrated process regulated by multiple proteins and signalling pathways. Cytokines constitute a major class of regulators of skeletal myogenesis. It is well established that infiltrating immune cells at the site of muscle injury secrete cytokines, which play critical roles in the myofibre repair and regeneration process. In the past 10-15 years, skeletal muscle itself has emerged as a prolific producer of cytokines. Much attention in the field has been focused on the endocrine effects of muscle-secreted cytokines (myokines) on metabolic regulation. However, ample evidence suggests that muscle-derived cytokines also regulate myogenic differentiation and muscle regeneration in an autocrine manner. In this review, we survey cytokines that meet two criteria: (a) evidence of expression by muscle cells; (b) evidence demonstrating a myogenic function. Dozens of cytokines representing several major classes make up this group, and together they regulate all steps of the myogenic process. How such a large array of cytokines coordinate their signalling to form a regulatory network is a fascinating, pressing question. Functional studies that can distinguish the source of the cytokines in vivo are also much needed in order to facilitate exploration of their full therapeutic potential.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据