Reloading functionally ameliorates disuse-induced muscle atrophy by reversing mitochondrial dysfunction, and similar benefits are gained by administering a combination of mitochondrial nutrients

Liu, Jing; Peng, Yunhua; Feng, Zhihui; Shi, Wen; Qu, Lei; Li, Yinghui; Liu, Jiankang; Long, Jiangang

doi:10.1016/j.freeradbiomed.2014.01.003

Cited by 46 publications

(59 citation statements)

References 41 publications

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“…For example, a large fall of PGC‐1α mRNA was observed just 1 d after nerve section in rat gastrocnemius muscle (29). Recently, Liu et al reported that reloading rat soleus muscle unloaded for 3 wk resulted a partial reversal of fiber CSA and mitochondrial deterioration, as well as prevention of unloading‐induced muscle ring finger‐1 and Atrogin‐1, and these findings were accompanied by an elevation of PGC‐1α and NRF‐1 (12). Because of the differences in species (rat vs. mouse), unloading model (hindlimb suspension vs. banding), and muscle phenotype (soleus vs. TA), the results of that study cannot be directly compared with our data.…”

Section: Discussionmentioning

confidence: 99%

PGC‐1α overexpression by in vivo transfection attenuates mitochondrial deterioration of skeletal muscle caused by immobilization

et al. 2015

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Prolonged immobilization (IM) causes skeletal muscle atrophy characterized by mitochondrial deterioration and proteolysis. Muscle remobilization (RM) increases reactive oxygen species generation, proinflammatory cytokine expression, and oxidative stress, preventing muscle from quick recovery. Thus, we hypothesized that overexpression of peroxisome proliferatoractivated receptor g coactivator 1-a (PGC-1a) via in vivo transfection would promote mitochondrial biogenesis and antioxidant defense, thus ameliorating the aforementioned deteriorations in a mouse model with 14-d IM followed by 5-d RM. PGC-1a transfection in tibialis anterior muscle resulted in a 7.2-and 4-fold increase in PGC-1a content in cytosol and nucleus, respectively. Mitochondrial biogenic (cytochrome c, mitochondrial transcription factor A), morphologic (mitochondrial density, mDNA/ nDNA ratio), and functional (cytochrome c oxidase activity, ATP synthesis rate) markers, as well as fiber crosssectional area, significantly increased in IM-RM muscle by PGC-1a overexpression. These effects were accompanied by an 18% decrease in H 2 O 2 , 30% decrease in nuclear factor-kB-DNA binding, and 25% reduction of IL-1b and-6 production in IM-RM muscle. There was a 34% increase in superoxide dismutase-2 activity, along with a 3.5-fold increase in NAD-dependent deacetylase sirtuin-3 expression caused by enhanced PGC-1a-estrogen-related receptor a binding. Our findings highlighted the importance of PGC1a in protecting muscle from metabolic and redox disturbances caused by IM.-Kang, C., Goodman, C. A., Horberger, T. A., Ji, L. L. PGC-1a overexpression by in vivo transfection attenuates mitochondrial deterioration of skeletal muscle caused by immobilization. FASEB J. 29, 4092-4106 (2015). www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

PGC‐1α overexpression by in vivo transfection attenuates mitochondrial deterioration of skeletal muscle caused by immobilization

et al. 2015

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“…Extra virgin olive oil, an integral ingredient of “Mediterranean diet,” benefits the risk of mild cognitive impairment and AD . We and others characterized that hydroxytyrosol (2‐(3,4‐di‐hydroxyphenyl)‐ethanol, HT), a major antioxidant phenolic in olive oil, effectively ameliorates oxidative stress, mitochondrial dysfunction, and neural toxicity in kinds of diseases [, ]. Although several studies have indicated the vital role of HT in modulating mitochondrial function in various disease models, studies on how HT regulates mitochondria in AD remains limited evidence.…”

Section: Introductionmentioning

confidence: 99%

Hydroxytyrosol mildly improve cognitive function independent of APP processing in APP/PS1 mice

Peng

Hou

Yang

et al. 2016

Molecular Nutrition Food Res

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“…These molecular alterations point toward a temporal induction of mitophagy both acutely and after 8 d of recovery after disuse. Nevertheless, previous data suggest a normalization of mitochondrial content upon several days of RL (34,(73)(74)(75), likely driven by an increase in mitochondrial biogenesis (34,73). The induction of mitophagy in the presence of a recovery of mitochondrial content suggests the induction of mitochondrial remodeling during remobilization.…”

Section: Discussionmentioning

confidence: 92%

Coordinated regulation of skeletal muscle mass and metabolic plasticity during recovery from disuse

et al. 2018

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Skeletal muscle regeneration after disuse is essential for muscle maintenance and involves the regulation of both mass- and metabolic plasticity-related processes. However, the relation between these processes during recovery from disuse remains unclear. In this study, we explored the potential interrelationship between the molecular regulation of muscle mass and oxidative metabolism during recovery from disuse. Molecular profiles were measured in biopsies from the vastus lateralis of healthy men after 1-leg cast immobilization and after 1 wk reloading, and in mouse gastrocnemius obtained before and after hindlimb suspension and during reloading (RL-1, -2, -3, -5, and -8 d). Cluster analysis of the human recovery response revealed correlations between myogenesis and autophagy markers in 2 clusters, which were distinguished by the presence of markers of early myogenesis, autophagosome formation, and mitochondrial turnover vs. markers of late myogenesis, autophagy initiation, and mitochondrial mass. In line with these findings, an early transient increase in B-cell lymphoma-2 interacting protein-3 and sequestosome-1 protein, and GABA type A receptor-associated protein like-1 protein and mRNA and a late increase in myomaker and myosin heavy chain-8 mRNA, microtubule-associated protein 1 light chain 3-II:I ratio, and FUN14 domain-containing-1 mRNA and protein were observed in mice. In summary, the regulatory profiles of protein, mitochondrial, and myonuclear turnover are correlated and temporally associated, suggesting a coordinated regulation of muscle mass- and oxidative metabolism-related processes during recovery from disuse.-Kneppers, A., Leermakers, P., Pansters, N., Backx, E., Gosker, H., van Loon, L., Schols, A., Langen, R., Verdijk, L. Coordinated regulation of skeletal muscle mass and metabolic plasticity during recovery from disuse.

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Reloading functionally ameliorates disuse-induced muscle atrophy by reversing mitochondrial dysfunction, and similar benefits are gained by administering a combination of mitochondrial nutrients

Cited by 46 publications

References 41 publications

PGC‐1α overexpression by in vivo transfection attenuates mitochondrial deterioration of skeletal muscle caused by immobilization

PGC‐1α overexpression by in vivo transfection attenuates mitochondrial deterioration of skeletal muscle caused by immobilization

Hydroxytyrosol mildly improve cognitive function independent of APP processing in APP/PS1 mice

Coordinated regulation of skeletal muscle mass and metabolic plasticity during recovery from disuse

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