This study investigates the role of the mitochondrial ATP-dependent potassium channel (mitoK<sub>ATP</sub>) in regulating skeletal muscle structure and function. The research explores how mitoK<sub>ATP</sub> activity influences mitochondrial morphology, energy metabolism, and muscle performance.
Deletion of Mitok in skeletal muscle led to altered mitochondrial cristae structure, impaired oxidative metabolism, reduced exercise capacity, and increased susceptibility to muscle damage. Conversely, overexpression of Mitok caused mitochondrial dysfunction, energy deficits, and muscle atrophy, indicating that proper regulation of mitoK<sub>ATP</sub> activity is essential for maintaining skeletal muscle homeostasis.
The study utilized both Knockout and overexpression mouse models to assess the function of mitoK<sub>ATP</sub> in skeletal muscle. The Knockout model involved deletion of the Mitok gene, encoding the pore-forming subunit of mitoK<sub>ATP</sub>, while the overexpression model involved increased expression of Mitok specifically in skeletal muscle tissues.
Mitochondrial function, Skeletal muscle physiology, Energy metabolism, Muscle atrophy, Exercise performance
Gene Knockout, Tissue-specific overexpression, Mitochondrial morphology analysis, Metabolic assessments, Muscle function tests
From model design to experimental results
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