scholarly journals Effect of Exercise Intensity on Unfolded Protein Response in Skeletal Muscle of Rat

2014 ◽  
Vol 18 (3) ◽  
pp. 211 ◽  
Author(s):  
Kihoon Kim ◽  
Yun-Hye Kim ◽  
Sung-Hye Lee ◽  
Man-Joong Jeon ◽  
So-Young Park ◽  
...  
2021 ◽  
Vol 22 (5) ◽  
pp. 2567
Author(s):  
Yann S. Gallot ◽  
Kyle R. Bohnert

Skeletal muscle is an essential organ, responsible for many physiological functions such as breathing, locomotion, postural maintenance, thermoregulation, and metabolism. Interestingly, skeletal muscle is a highly plastic tissue, capable of adapting to anabolic and catabolic stimuli. Skeletal muscle contains a specialized smooth endoplasmic reticulum (ER), known as the sarcoplasmic reticulum, composed of an extensive network of tubules. In addition to the role of folding and trafficking proteins within the cell, this specialized organelle is responsible for the regulated release of calcium ions (Ca2+) into the cytoplasm to trigger a muscle contraction. Under various stimuli, such as exercise, hypoxia, imbalances in calcium levels, ER homeostasis is disturbed and the amount of misfolded and/or unfolded proteins accumulates in the ER. This accumulation of misfolded/unfolded protein causes ER stress and leads to the activation of the unfolded protein response (UPR). Interestingly, the role of the UPR in skeletal muscle has only just begun to be elucidated. Accumulating evidence suggests that ER stress and UPR markers are drastically induced in various catabolic stimuli including cachexia, denervation, nutrient deprivation, aging, and disease. Evidence indicates some of these molecules appear to be aiding the skeletal muscle in regaining homeostasis whereas others demonstrate the ability to drive the atrophy. Continued investigations into the individual molecules of this complex pathway are necessary to fully understand the mechanisms.


2017 ◽  
Vol 6 (7) ◽  
pp. 621-630 ◽  
Author(s):  
Petter S. Alm ◽  
Thais de Castro Barbosa ◽  
Romain Barrès ◽  
Anna Krook ◽  
Juleen R. Zierath

2020 ◽  
Vol 318 (4) ◽  
pp. R677-R690 ◽  
Author(s):  
Yuka Wakabayashi ◽  
Yuki Tamura ◽  
Karina Kouzaki ◽  
Naoki Kikuchi ◽  
Kenji Hiranuma ◽  
...  

Acetaldehyde dehydrogenase 2 (ALDH2) is an enzyme involved in redox homeostasis as well as the detoxification process in alcohol metabolism. Nearly 8% of the world’s population have an inactivating mutation in the ALDH2 gene. However, the expression patterns and specific functions of ALDH2 in skeletal muscles are still unclear. Herein, we report that ALDH2 is expressed in skeletal muscle and is localized to the mitochondrial fraction. Oxidative muscles had a higher amount of ALDH2 protein than glycolytic muscles. We next comprehensively investigated whether ALDH2 knockout in mice induces mitochondrial adaptations in gastrocnemius muscle (for example, content, enzymatic activity, respiratory function, supercomplex formation, and functional networking). We found that ALDH2 deficiency resulted in partial mitochondrial dysfunction in gastrocnemius muscle because it increased mitochondrial reactive oxygen species (ROS) emission (2′,7′-dichlorofluorescein and MitoSOX oxidation rate during respiration) and the frequency of regional mitochondrial depolarization. Moreover, we determined whether ALDH2 deficiency and the related mitochondrial dysfunction trigger mitochondrial stress and quality control responses in gastrocnemius muscle (for example, mitophagy markers, dynamics, and the unfolded protein response). We found that ALDH2 deficiency upregulated the mitochondrial serine protease Omi/HtrA2 (a marker of the activation of a branch of the mitochondrial unfolded protein response). In summary, ALDH2 deficiency leads to greater mitochondrial ROS production, but homeostasis can be maintained via an appropriate stress response.


Aging ◽  
2019 ◽  
Vol 11 (18) ◽  
pp. 7587-7604 ◽  
Author(s):  
Corey R. Hart ◽  
Zachary C. Ryan ◽  
Kyle T. Pfaffenbach ◽  
Surendra Dasari ◽  
Mojtaba Parvizi ◽  
...  

2011 ◽  
Vol 13 (2) ◽  
pp. 160-169 ◽  
Author(s):  
Jun Wu ◽  
Jorge L. Ruas ◽  
Jennifer L. Estall ◽  
Kyle A. Rasbach ◽  
Jang Hyun Choi ◽  
...  

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