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Abstract
Overexpression of Miro1 improved muscle fiber count and cross-sectional area in a mouse model of muscle atrophy.
- Mitochondrial dysfunction is linked to muscle atrophy, which involves loss of skeletal muscle mass and function.
- Miro1 is essential for mitochondrial transfer via tunneling nanotubes, influencing mitochondrial movement and health.
- In vitro, overexpression of Milton did not enhance mitochondrial transfer in muscle cells without Miro1.
- Miro1 knockdown significantly reduced mitochondrial transfer in vivo, while its overexpression improved mitochondrial morphology.
- Miro1 overexpression also upregulated collagen types I/III and downregulated muscle atrophy markers Atrogin1 and MURF1.
- Functional improvements included increased grip strength, running distance, and elevated levels of proteins related to mitochondrial health.
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