Absence of physiological Ca²⁺ transients is an initial trigger for mitochondrial dysfunction in skeletal muscle following denervation.

ABSTRACT:

Background

Motor neurons control muscle contraction by initiating action potentials in muscle. Denervation of muscle from motor neurons leads to muscle atrophy, which is linked to mitochondrial dysfunction. It is known that denervation promotes mitochondrial reactive oxygen species (ROS) production in muscle, whereas the initial cause of mitochondrial ROS production in denervated muscle remains elusive. Since denervation isolates muscle from motor neurons and deprives it from any electric stimulation, no action potentials are initiated, and therefore, no physiological Ca²⁺ transients are generated inside denervated muscle fibers. We tested whether loss of physiological Ca²⁺ transients is an initial cause leading to mitochondrial dysfunction in denervated skele

SUBMITTER: Karam C 

PROVIDER: S-EPMC5387329 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature