Franco-Romero Anais, Sandri Marco, Schiaffino Stefano
Veneto Institute of Molecular Medicine, 35129 Padova, Italy.
Department of Biomedical Sciences, University of Padova, 35121 Padova, Italy.
Cold Spring Harb Perspect Biol. 2025 Jun 2;17(6):a041565. doi: 10.1101/cshperspect.a041565.
Skeletal muscle fibers possess, like all cells of our body, an evolutionary conserved autophagy machinery, which allows them to segregate unfolded proteins and damaged organelles within autophagosomes, and to induce fusion of autophagosomes with lysosomes, leading to degradation of those altered cell constituents. This process may be selective for specific cell components, as in the case of glycogen (glycophagy) or organelles, as with mitochondria (mitophagy). The autophagic flux is activated by fasting, and contributes with the proteasome to provide the organism with amino acids required for survival. Autophagy is also essential for the normal turnover of muscle proteins and organelles, as shown by the degenerative changes induced by genetic block of the autophagic mechanism, and in several myopathies. Autophagy is enhanced in muscle by exercise and impaired during aging, suggesting that aging-dependent muscle dysfunction could be delayed by boosting autophagy.
骨骼肌纤维与我们身体的所有细胞一样,拥有一种进化上保守的自噬机制,该机制使它们能够在自噬体内分离未折叠的蛋白质和受损的细胞器,并诱导自噬体与溶酶体融合,从而导致这些改变的细胞成分降解。这个过程可能对特定的细胞成分具有选择性,比如糖原(糖原自噬)或细胞器,如线粒体(线粒体自噬)。自噬通量在禁食时被激活,并与蛋白酶体共同作用,为生物体提供生存所需的氨基酸。自噬对于肌肉蛋白质和细胞器的正常更新也至关重要,这在自噬机制的基因阻断以及多种肌病所引发的退行性变化中得到了体现。运动可增强肌肉中的自噬,而衰老过程中自噬会受损,这表明通过增强自噬可以延缓与衰老相关的肌肉功能障碍。