Diminished force production and mitochondrial respiratory deficits are strain-dependent myopathies of subacute limb ischemia.

ABSTRACT:

Objective

Reduced skeletal muscle mitochondrial function might be a contributing mechanism to the myopathy and activity based limitations that typically plague patients with peripheral arterial disease (PAD). We hypothesized that mitochondrial dysfunction, myofiber atrophy, and muscle contractile deficits are inherently determined by the genetic background of regenerating ischemic mouse skeletal muscle, similar to how patient genetics affect the distribution of disease severity with clinical PAD.

Methods

Genetically ischemia protected (C57BL/6) and susceptible (BALB/c) mice underwent either unilateral subacute hind limb ischemia (SLI) or myotoxic injury (cardiotoxin) for 28 days. Limbs were monitored for blood flow and tissue oxygen saturation and tissue was collected for th

SUBMITTER: Schmidt CA 

PROVIDER: S-EPMC5403600 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature