scholarly journals Skeletal muscle aging: influence of oxidative stress and physical exercise

Oncotarget ◽  
2017 ◽  
Vol 8 (12) ◽  
pp. 20428-20440 ◽  
Author(s):  
Mariana Janini Gomes ◽  
Paula Felippe Martinez ◽  
Luana Urbano Pagan ◽  
Ricardo Luiz Damatto ◽  
Marcelo Diacardia Mariano Cezar ◽  
...  
Life Sciences ◽  
2020 ◽  
Vol 252 ◽  
pp. 117630 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Yan-Zhong Chang

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Yun-Fei Yang ◽  
Wu Yang ◽  
Zhi-Yin Liao ◽  
Yong-Xin Wu ◽  
Zhen Fan ◽  
...  

AbstractAge-related loss of skeletal muscle mass and function, termed sarcopenia, could impair the quality of life in the elderly. The mechanisms involved in skeletal muscle aging are intricate and largely unknown. However, more and more evidence demonstrated that mitochondrial dysfunction and apoptosis also play an important role in skeletal muscle aging. Recent studies have shown that mitochondrial calcium uniporter (MCU)-mediated mitochondrial calcium affects skeletal muscle mass and function by affecting mitochondrial function. During aging, we observed downregulated expression of mitochondrial calcium uptake family member3 (MICU3) in skeletal muscle, a regulator of MCU, which resulted in a significant reduction in mitochondrial calcium uptake. However, the role of MICU3 in skeletal muscle aging remains poorly understood. Therefore, we investigated the effect of MICU3 on the skeletal muscle of aged mice and senescent C2C12 cells induced by d-gal. Downregulation of MICU3 was associated with decreased myogenesis but increased oxidative stress and apoptosis. Reconstitution of MICU3 enhanced antioxidants, prevented the accumulation of mitochondrial ROS, decreased apoptosis, and increased myogenesis. These findings indicate that MICU3 might promote mitochondrial Ca2+ homeostasis and function, attenuate oxidative stress and apoptosis, and restore skeletal muscle mass and function. Therefore, MICU3 may be a potential therapeutic target in skeletal muscle aging.


2018 ◽  
Vol Volume 13 ◽  
pp. 2407-2419 ◽  
Author(s):  
Yan Zheng ◽  
Jian Kong ◽  
Qun Li ◽  
Yan Wang ◽  
Jie Li

2020 ◽  
Vol 21 (15) ◽  
pp. 5236 ◽  
Author(s):  
Evelyn Ferri ◽  
Emanuele Marzetti ◽  
Riccardo Calvani ◽  
Anna Picca ◽  
Matteo Cesari ◽  
...  

Skeletal muscle aging is associated with a significant loss of skeletal muscle strength and power (i.e., dynapenia), muscle mass and quality of life, a phenomenon known as sarcopenia. This condition affects nearly one-third of the older population and is one of the main factors leading to negative health outcomes in geriatric patients. Notwithstanding the exact mechanisms responsible for sarcopenia are not fully understood, mitochondria have emerged as one of the central regulators of sarcopenia. In fact, there is a wide consensus on the assumption that the loss of mitochondrial integrity in myocytes is the main factor leading to muscle degeneration. Mitochondria are also key players in senescence. It has been largely proven that the modulation of mitochondrial functions can induce the death of senescent cells and that removal of senescent cells improves musculoskeletal health, quality, and function. In this review, the crosstalk among mitochondria, cellular senescence, and sarcopenia will be discussed with the aim to elucidate the role that the musculoskeletal cellular senescence may play in the onset of sarcopenia through the mediation of mitochondria.


Bone ◽  
2019 ◽  
Vol 127 ◽  
pp. 26-36 ◽  
Author(s):  
Zaira Aversa ◽  
Xu Zhang ◽  
Roger A. Fielding ◽  
Ian Lanza ◽  
Nathan K. LeBrasseur

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