The mitochondrial ATP-dependent potassium channel (mitoKATP) controls skeletal muscle structure and function

DiMarco G
January 17, 2024
Cell Death Dis
https://pubmed.ncbi.nlm.nih.gov/38233399

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/38233399

Research summary

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.

Key outcome of the study

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.

Mouse model

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.

TARGET:
Mitok
Mitochondrial ATP-dependent potassium channel pore-forming subunit

Keywords

Mitochondrial function, Skeletal muscle physiology, Energy metabolism, Muscle atrophy, Exercise performance

Technical specifications

Gene Knockout, Tissue-specific overexpression, Mitochondrial morphology analysis, Metabolic assessments, Muscle function tests

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Constitutive KO mouse

A constitutive, conventional, or whole-body Knockout mouse is a fast and cost-effective solution for in vivo preliminary studies of target gene functions.