RRC ID 27888
著者 Grumati P, Coletto L, Schiavinato A, Castagnaro S, Bertaggia E, Sandri M, Bonaldo P.
タイトル Physical exercise stimulates autophagy in normal skeletal muscles but is detrimental for collagen VI-deficient muscles.
ジャーナル Autophagy
Abstract Autophagy is a catabolic process that provides the degradation of altered/damaged organelles through the fusion between autophagosomes and lysosomes. Proper regulation of the autophagic flux is fundamental for the homeostasis of skeletal muscles in physiological conditions and in response to stress. Defective as well as excessive autophagy is detrimental for muscle health and has a pathogenic role in several forms of muscle diseases. Recently, we found that defective activation of the autophagic machinery plays a key role in the pathogenesis of muscular dystrophies linked to collagen VI. Impairment of the autophagic flux in collagen VI null (Col6a1–/–) mice causes accumulation of dysfunctional mitochondria and altered sarcoplasmic reticulum, leading to apoptosis and degeneration of muscle fibers. Here we show that physical exercise activates autophagy in skeletal muscles. Notably, physical training exacerbated the dystrophic phenotype of Col6a1–/– mice, where autophagy flux is compromised. Autophagy was not induced in Col6a1–/– muscles after either acute or prolonged exercise, and this led to a marked increase of muscle wasting and apoptosis. These findings indicate that proper activation of autophagy is important for muscle homeostasis during physical activity.
巻・号 7(12)
ページ 1415-23
公開日 2011-12-1
DOI 10.4161/auto.7.12.17877
PII 17877
PMID 22024752
PMC PMC3288016
MeSH Animals Autophagy* Collagen Type VI / deficiency* Collagen Type VI / metabolism Mice Mice, Inbred C57BL Muscle, Skeletal / metabolism* Muscle, Skeletal / pathology* Muscle, Skeletal / ultrastructure Physical Conditioning, Animal* Time Factors Wasting Syndrome / pathology
IF 9.77
引用数 141
WOS 分野 CELL BIOLOGY
リソース情報
実験動物マウス RBRC00806