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Eshima 2020 J Appl Physiol (1985)

From Bioblast
Publications in the MiPMap
Eshima H, Siripoksup P, Mahmassani ZS, Johnson JM, Ferrara PJ, Verkerke ARP, Salcedo A, Drummond MJ, Funai K (2020) Neutralizing mitochondrial ROS does not rescue muscle atrophy induced by hindlimb unloading in female mice. J Appl Physiol (1985) 129:124-32.

Β» PMID: 32552434

Eshima Hiroaki, Siripoksup Piyarat, Mahmassani Ziad S, Johnson Jordan M, Ferrara Patrick J, Verkerke Anthony R P, Salcedo Anahy, Drummond Micah J, Funai Katsuhiko (2020) J Appl Physiol (1985)

Abstract: Excess reactive oxygen species (ROS) induced by physical inactivity is associated with muscle atrophy and muscle weakness. However, the role of mitochondrial ROS on disuse-induced muscle atrophy is not fully understood. The purpose of this study was to utilize a genetic strategy to examine the effect of neutralizing mitochondrial ROS on disuse-induced skeletal muscle atrophy. This was accomplished by placing wildtype (WT) and mitochondrial-targeted catalase expressing (MCAT) littermate mice on 7-days of hindlimb unloading. After assessment of body weight and composition, muscles were analyzed for individual muscle mass, force generating capacity, fiber-type, cross-sectional area, and mitochondrial phenotyping including H2O2 production. Despite a successful attenuation of mitochondrial ROS, MCAT mice were not protected from muscle atrophy. No differences were observed in body composition, lean mass, individual muscle masses, force-generating capacity, and muscle fiber cross-sectional area. These data suggest that neutralizing mitochondrial ROS is insufficient to suppress disuse-induced loss of skeletal muscle mass and contractile function. β€’ Keywords: Mitochondria, Oxidative stress, Reactive oxygen species, Hindlimb-unloading, Muscle atrophy β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: US UT Salt Lake City Funai K

Labels: MiParea: Respiration 

Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria 

Coupling state: LEAK, OXPHOS, ET  Pathway: N, NS  HRR: Oxygraph-2k