Journal of cellular physiology, 2021-11, Vol.236 (11), p.7612-7624
2021
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Details
- Autor(en) / Beteiligte
- Titel
- Mitophagy reporter mouse analysis reveals increased mitophagy activity in disuse‐induced muscle atrophy
- Ist Teil von
- Journal of cellular physiology, 2021-11, Vol.236 (11), p.7612-7624
- Ort / Verlag
- United States: Wiley Subscription Services, Inc
- Erscheinungsjahr
- 2021
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Muscle disuse induces atrophy through increased reactive oxygen species (ROS) released from damaged mitochondria. Mitophagy, the autophagic degradation of mitochondria, is associated with increased ROS production. However, the mitophagy activity status during disuse‐induced muscle atrophy has been a subject of debate. Here, we developed a new mitophagy reporter mouse line to examine how disuse affected mitophagy activity in skeletal muscles. Mice expressing tandem mCherry‐EGFP proteins on mitochondria were then used to monitor the dynamics of mitophagy activity. The reporter mice demonstrated enhanced mitophagy activity and increased ROS production in atrophic soleus muscles following a 14‐day hindlimb immobilization. Results also showed an increased expression of multiple mitophagy genes, including Bnip3, Bnip3l, and Park2. Our findings thus conclude that disuse enhances mitophagy activity and ROS production in atrophic skeletal muscles and suggests that mitophagy is a potential therapeutic target for disuse‐induced muscle atrophy. Disuse‐induced muscle atrophy is associated with increased reactive oxygen species (ROS) from damaged mitochondria and mitophagy activity. However, the mitophagy activity status during disuse‐induced muscle atrophy has been a subject of debate. In this study, we create a new line of mitophagy reporter mouse to examine the status of mitophagy activity in atrophic skeletal muscles. Our study concludes that disuse enhances mitophagy activity as well as ROS production in atrophic muscles.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0021-9541eISSN: 1097-4652DOI: 10.1002/jcp.30404Titel-ID: cdi_proquest_miscellaneous_2521493040
- Format
- –
- Schlagworte
- Adaptor Proteins, Signal Transducing - genetics, Adaptor Proteins, Signal Transducing - metabolism, Animals, Atrophy, BNIP3 protein, Disease Models, Animal, disuse‐induced muscle atrophy, Gene expression, Green Fluorescent Proteins - genetics, Green Fluorescent Proteins - metabolism, hindlimb immobilization, Hindlimb Suspension, Immobilization, Luminescent Proteins - genetics, Luminescent Proteins - metabolism, Membrane Proteins - genetics, Membrane Proteins - metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Mitochondria, Heart - genetics, Mitochondria, Heart - metabolism, Mitochondria, Heart - pathology, Mitochondria, Muscle - genetics, Mitochondria, Muscle - metabolism, Mitochondria, Muscle - pathology, Mitophagy, Muscle, Skeletal - metabolism, Muscle, Skeletal - pathology, Muscles, Muscular Atrophy - genetics, Muscular Atrophy - metabolism, Muscular Atrophy - pathology, Myocardium - metabolism, Myocardium - pathology, Reactive oxygen species, Reactive Oxygen Species - metabolism, Red Fluorescent Protein, ROS, Signal Transduction, Skeletal muscle, Starvation, Therapeutic targets, Time Factors