Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching.

ABSTRACT:

Background

Excess reactive oxygen species (ROS) and muscle weakness occur in parallel in multiple pathological conditions. However, the causative role of skeletal muscle mitochondrial ROS (mtROS) on neuromuscular junction (NMJ) morphology and function and muscle weakness has not been directly investigated.

Methods

We generated mice lacking skeletal muscle-specific manganese-superoxide dismutase (mSod2KO) to increase mtROS using a cre-Lox approach driven by human skeletal actin. We determined primary functional parameters of skeletal muscle mitochondrial function (respiration, ROS, and calcium retention capacity) using permeabilized muscle fibres and isolated muscle mitochondria. We assessed contractile properties of isolated skeletal muscle using in situ and in vitro prepara

SUBMITTER: Ahn B 

PROVIDER: S-EPMC6463475 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature