Astaxanthin supplementation attenuates disuse muscle atrophy and myonuclear apoptosis in rat skeletal muscle

2018 ◽  
Vol 3 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Rat Skeletal Muscle ◽  
Disuse Muscle Atrophy

scholarly journals FOXO signaling is required for disuse muscle atrophy and is directly regulated by Hsp70

2010 ◽  
Vol 298 (1) ◽  
pp. C38-C45 ◽  
Author(s):  
Sarah M. Senf ◽  
Stephen L. Dodd ◽  
Andrew R. Judge
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Fiber ◽  
Muscle Wasting ◽  
Dominant Negative ◽  
Disuse Muscle Atrophy ◽  
Rat Soleus Muscle ◽  
Muscle Fiber Atrophy ◽  
Fiber Atrophy

The purpose of the current study was to determine whether heat shock protein 70 (Hsp70) directly regulates forkhead box O (FOXO) signaling in skeletal muscle. This aim stems from previous work demonstrating that Hsp70 overexpression inhibits disuse-induced FOXO transactivation and prevents muscle fiber atrophy. However, although FOXO is sufficient to cause muscle wasting, no data currently exist on the requirement of FOXO signaling in the progression of physiological muscle wasting, in vivo. In the current study we show that specific inhibition of FOXO, via expression of a dominant-negative FOXO3a, in rat soleus muscle during disuse prevented >40% of muscle fiber atrophy, demonstrating that FOXO signaling is required for disuse muscle atrophy. Subsequent experiments determined whether Hsp70 directly regulates FOXO3a signaling when independently activated in skeletal muscle, via transfection of FOXO3a. We show that Hsp70 inhibits FOXO3a-dependent transcription in a gene-specific manner. Specifically, Hsp70 inhibited FOXO3a-induced promoter activation of atrogin-1, but not MuRF1. Further studies showed that a FOXO3a DNA-binding mutant can activate MuRF1, but not atrogin-1, suggesting that FOXO3a activates these two genes through differential mechanisms. In summary, FOXO signaling is required for physiological muscle atrophy and is directly inhibited by Hsp70.

scholarly journals Various Jobs of Proteolytic Enzymes in Skeletal Muscle during Unloading: Facts and Speculations

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
E. V. Kachaeva ◽  
B. S. Shenkman
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Skeletal Muscles ◽  
Proteolytic Enzymes ◽  
Disuse Atrophy ◽  
Muscle Degeneration ◽  
Muscle Adaptation ◽  
Signaling Systems ◽  
Disuse Muscle Atrophy ◽  
Postural Muscles

Skeletal muscles, namely, postural muscles, as soleus, suffer from atrophy under disuse. Muscle atrophy development caused by unloading differs from that induced by denervation or other stimuli. Disuse atrophy is supposed to be the result of shift of protein synthesis/proteolysis balance towards protein degradation increase. Maintaining of the balance involves many systems of synthesis and proteolysis, whose activation leads to muscle adaptation to disuse rather than muscle degeneration. Here, we review recent data on activity of signaling systems involved in muscle atrophy development under unloading and muscle adaptation to the lack of support.

scholarly journals Mitochondrial signaling contributes to disuse muscle atrophy

2012 ◽  
Vol 303 (1) ◽  
pp. E31-E39 ◽  
Author(s):  
Scott K. Powers ◽  
Michael P. Wiggs ◽  
Jose A. Duarte ◽  
A. Murat Zergeroglu ◽  
Haydar A. Demirel
Keyword(s):  
Skeletal Muscle ◽  
Mechanical Ventilation ◽  
Muscle Atrophy ◽  
Prolonged Mechanical Ventilation ◽  
Therapeutic Interventions ◽  
Skeletal Muscle Atrophy ◽  
Future Research ◽  
Primary Role ◽  
Mitochondrial Signaling ◽  
Disuse Muscle Atrophy

It is well established that long durations of bed rest, limb immobilization, or reduced activity in respiratory muscles during mechanical ventilation results in skeletal muscle atrophy in humans and other animals. The idea that mitochondrial damage/dysfunction contributes to disuse muscle atrophy originated over 40 years ago. These early studies were largely descriptive and did not provide unequivocal evidence that mitochondria play a primary role in disuse muscle atrophy. However, recent experiments have provided direct evidence connecting mitochondrial dysfunction to muscle atrophy. Numerous studies have described changes in mitochondria shape, number, and function in skeletal muscles exposed to prolonged periods of inactivity. Furthermore, recent evidence indicates that increased mitochondrial ROS production plays a key signaling role in both immobilization-induced limb muscle atrophy and diaphragmatic atrophy occurring during prolonged mechanical ventilation. Moreover, new evidence reveals that, during denervation-induced muscle atrophy, increased mitochondrial fragmentation due to fission is a required signaling event that activates the AMPK-FoxO3 signaling axis, which induces the expression of atrophy genes, protein breakdown, and ultimately muscle atrophy. Collectively, these findings highlight the importance of future research to better understand the mitochondrial signaling mechanisms that contribute to disuse muscle atrophy and to develop novel therapeutic interventions for prevention of inactivity-induced skeletal muscle atrophy.

Immobilization-induced activation of key proteolytic systems in skeletal muscles is prevented by a mitochondria-targeted antioxidant

2013 ◽  
Vol 115 (4) ◽  
pp. 529-538 ◽  
Author(s):  
Erin E. Talbert ◽  
Ashley J. Smuder ◽  
Kisuk Min ◽  
Oh Sung Kwon ◽  
Hazel H. Szeto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Skeletal Muscles ◽  
Mammalian Target Of Rapamycin ◽  
Skeletal Muscle Atrophy ◽  
Muscle Disuse ◽  
Mitochondrial Ros ◽  
Disuse Muscle Atrophy ◽  
Muscle Fiber Atrophy ◽  
First Time

Long periods of skeletal muscle disuse result in muscle fiber atrophy, and mitochondrial production of reactive oxygen species (ROS) appears to be a required signal for the increase in protein degradation that occurs during disuse muscle atrophy. The experiments detailed here demonstrate for the first time in limb muscle that the inactivity-induced increases in E3 ligase expression and autophagy biomarkers result from increases in mitochondrial ROS emission. Treatment of animals with a mitochondrial-targeted antioxidant also prevented the disuse-induced decrease in anabolic signaling (Akt/mammalian target of rapamycin signaling) that is normally associated with prolonged inactivity in skeletal muscles. Additionally, our results confirm previous findings that treatment with a mitochondrial-targeted antioxidant is sufficient to prevent casting-induced skeletal muscle atrophy, mitochondrial dysfunction, and activation of the proteases calpain and caspase-3. Collectively, these data reveal that inactivity-induced increases in mitochondrial ROS emission play a required role in activation of key proteolytic systems and the downregulation of important anabolic signaling molecules in muscle fibers exposed to prolonged inactivity.

scholarly journals Effects of exercise on AKT/PGC1-α/FOXO3a pathway and muscle atrophy in cisplatin-administered rat skeletal muscle

2021 ◽  
Vol 25 (6) ◽  
pp. 585-592
Author(s):  
Jun Hyun Bae ◽  
Dae Yun Seo ◽  
Sang Ho Lee ◽  
Chaeyoung Shin ◽  
Parivash Jamrasi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Rat Skeletal Muscle

scholarly journals Low-frequency Electrical Stimulation Alleviates Immobilization-evoked Disuse Muscle Atrophy via Repressing Autophagy in Skeletal Muscle of Rabbits

2021 ◽  
Author(s):  
A-Ying Liu ◽  
Quan-Bing Zhang ◽  
Hua-Long Zhu ◽  
Yong-Wei Xiong ◽  
Feng Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Knee Joint ◽  
Muscle Atrophy ◽  
Rabbit Model ◽  
Low Frequency ◽  
Cross Sectional ◽  
Disuse Muscle Atrophy ◽  
Joint Range ◽  
Time Point

Abstract Objective: The present study was to investigate the effect of low-frequency electrical stimulation on disuse muscle atrophy and its mechanism in a rabbit model of extending knee joint contracture.Methods: This study designed two experiments. In the time-point experiment, 24 rabbits were randomly divided into Control 1(Ctrl1), immobilization for 2 weeks (I-2), I-4, and I-6 groups. In the intervention experiment, 24 rabbits were also randomly divided into Control 2 (Ctrl2), electrical stimulation (ES), natural recovery (NR) and electrical stimulation treatment (EST) groups. All intervention effects were assessed by evaluating the knee joint range of motion (ROM), cross-sectional area (CSA) of muscle and the expression of autophagy-related proteins.Results: Time-point experiment showed that immobilization reduced knee ROM, muscle CSA, and activated autophagy in skeletal muscle. Levels of four autophagic proteins including p-mTOR, Atg7, p62 and LC3B-II, were significantly elevated in the skeletal muscle of I-4 group. The intervention experiment further presented that LFES significantly improved the immobilization-induced ROM and CSA reduction. Additionally, LFES significantly reversed autophagy activation of skeletal muscle caused by immobilization.Conclusions: Low-frequency electrical stimulation alleviates immobilization-evoked disuse muscle atrophy maybe via inhibiting autophagy in skeletal muscle of rabbits.

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