scholarly journals Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease

2016 ◽  
Vol 6 ◽  
Author(s):  
Erick O. Hernández-Ochoa ◽  
Stephen J. P. Pratt ◽  
Richard M. Lovering ◽  
Martin F. Schneider
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Calcium Release ◽  
Critical Role ◽  
Skeletal Muscle Function ◽  
Calcium Release Channels

scholarly journals Impact of Intrinsic Muscle Weakness on Muscle–Bone Crosstalk in Osteogenesis Imperfecta

2021 ◽  
Vol 22 (9) ◽  
pp. 4963
Author(s):  
Victoria L. Gremminger ◽  
Charlotte L. Phillips
Keyword(s):  
Skeletal Muscle ◽  
Osteogenesis Imperfecta ◽  
Muscle Weakness ◽  
Muscle Function ◽  
Critical Role ◽  
Connective Tissue Disorder ◽  
Bone Fragility ◽  
Skeletal Muscle Function ◽  
Skeletal Muscle Weakness

Bone and muscle are highly synergistic tissues that communicate extensively via mechanotransduction and biochemical signaling. Osteogenesis imperfecta (OI) is a heritable connective tissue disorder of severe bone fragility and recently recognized skeletal muscle weakness. The presence of impaired bone and muscle in OI leads to a continuous cycle of altered muscle–bone crosstalk with weak muscles further compromising bone and vice versa. Currently, there is no cure for OI and understanding the pathogenesis of the skeletal muscle weakness in relation to the bone pathogenesis of OI in light of the critical role of muscle–bone crosstalk is essential to developing and identifying novel therapeutic targets and strategies for OI. This review will highlight how impaired skeletal muscle function contributes to the pathophysiology of OI and how this phenomenon further perpetuates bone fragility.

scholarly journals The role of SIRT1 in skeletal muscle function and repair of older mice

2019 ◽  
Vol 10 (4) ◽  
pp. 929-949 ◽  
Author(s):  
Matthew J. Myers ◽  
Danielle L. Shepherd ◽  
Andrya J. Durr ◽  
David S. Stanton ◽  
Junaith S. Mohamed ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function

Abstract 273: The Role of Estrogen in Protection of Skeletal Muscle Function in Diastolic Dysfunction

2019 ◽  
Vol 125 (Suppl_1) ◽  
Author(s):  
Somik Chatterjee ◽  
Shumin Li ◽  
Aijun Zhang ◽  
Indira Vedula ◽  
Judy A AlRukby ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Diastolic Dysfunction ◽  
Muscle Function ◽  
Skeletal Muscle Function

scholarly journals Role of p66shc in skeletal muscle function

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Veronica Granatiero ◽  
Gaia Gherardi ◽  
Matteo Vianello ◽  
Elsa Salerno ◽  
Erika Zecchini ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function

The role of sphingolipids in the control of skeletal muscle function: a review

1999 ◽  
Vol 20 (6) ◽  
pp. 423-430 ◽  
Author(s):  
R.A. Sabbadini ◽  
D. Danieli-Betto ◽  
R. Betto
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Skeletal Muscle Function

Disruption of muscle renin-angiotensin system in AT1a−/−mice enhances muscle function despite reducing muscle mass but compromises repair after injury

2012 ◽  
Vol 303 (3) ◽  
pp. R321-R331 ◽  
Author(s):  
Kate T. Murphy ◽  
Andrew M. Allen ◽  
Annabel Chee ◽  
Timur Naim ◽  
Gordon S. Lynch
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Function ◽  
Renin Angiotensin System ◽  
Whole Body ◽  
Ras Signaling ◽  
Skeletal Muscle Function ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system (RAS) in vasoregulation is well established, but a localized RAS exists in multiple tissues and exerts diverse functions including autonomic control and thermogenesis. The role of the RAS in the maintenance and function of skeletal muscle is not well understood, especially the role of angiotensin peptides, which appear to contribute to muscle atrophy. We tested the hypothesis that mice lacking the angiotensin type 1A receptor (AT1A−/−) would exhibit enhanced whole body and skeletal muscle function and improved regeneration after severe injury. Despite 18- to 20-wk-old AT1A−/−mice exhibiting reduced muscle mass compared with controls ( P < 0.05), the tibialis anterior (TA) muscles produced a 25% higher maximum specific (normalized) force ( P < 0.05). Average fiber cross-sectional area (CSA) and fiber oxidative capacity was not different between groups, but TA muscles from AT1A−/−mice had a reduced number of muscle fibers as well as a higher proportion of type IIx/b fibers and a lower proportion of type IIa fibers ( P < 0.05). Measures of whole body function (grip strength, rotarod performance, locomotor activity) were all improved in AT1A−/−mice ( P < 0.05). Surprisingly, the recovery of muscle mass and fiber CSA following myotoxic injury was impaired in AT1A−/−mice, in part by impaired myoblast fusion, prolonged collagen infiltration and inflammation, and delayed expression of myogenic regulatory factors. The findings support the therapeutic potential of RAS inhibition for enhancing whole body and skeletal muscle function, but they also reveal the importance of RAS signaling in the maintenance of muscle mass and for normal fiber repair after injury.

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