scholarly journals Regrowth after skeletal muscle atrophy is impaired in aged rats, despite similar responses in signaling pathways

2015 ◽  
Vol 64 ◽  
pp. 17-32 ◽  
Author(s):  
Jena R. White ◽  
Amy L. Confides ◽  
Stephanie Moore-Reed ◽  
Johanna M. Hoch ◽  
Esther E. Dupont-Versteegden
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Aged Rats

Myostatin and the skeletal muscle atrophy and hypertrophy signaling pathways

2014 ◽  
Vol 71 (22) ◽  
pp. 4361-4371 ◽  
Author(s):  
J. Rodriguez ◽  
B. Vernus ◽  
I. Chelh ◽  
I. Cassar-Malek ◽  
J. C. Gabillard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Atrophy And Hypertrophy

scholarly journals Leucine minimizes denervation-induced skeletal muscle atrophy of rats through akt/mtor signaling pathways

2015 ◽  
Vol 6 ◽  
Author(s):  
Carolina B. Ribeiro ◽  
Daiane C. Christofoletti ◽  
Vitor A. Pezolato ◽  
Rita de Cássia Marqueti Durigan ◽  
Jonato Prestes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Atrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Atrophy

scholarly journals Edward F. Adolph Distinguished Lecture. Skeletal muscle atrophy: Multiple pathways leading to a common outcome

2020 ◽  
Vol 129 (2) ◽  
pp. 272-282 ◽  
Author(s):  
Sue C. Bodine
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Skeletal Muscle Mass ◽  
Single Gene ◽  
Skeletal Muscle Atrophy ◽  
Protein Breakdown ◽  
E3 Ligases ◽  
The Past

Skeletal muscle atrophy continues to be a serious consequence of many diseases and conditions for which there is no treatment. Our understanding of the mechanisms regulating skeletal muscle mass has improved considerably over the past two decades. For many years it was known that skeletal muscle atrophy resulted from an imbalance between protein synthesis and protein breakdown, with the net balance shifting toward protein breakdown. However, the molecular and cellular mechanisms underlying the increased breakdown of myofibrils was unknown. Over the past two decades, numerous reports have identified novel genes and signaling pathways that are upregulated and activated in response to stimuli such as disuse, inflammation, metabolic stress, starvation and others that induce muscle atrophy. This review summarizes the discovery efforts performed in the identification of several pathways involved in the regulation of skeletal muscle mass: the mammalian target of rapamycin (mTORC1) and the ubiquitin proteasome pathway and the E3 ligases, MuRF1 and MAFbx. While muscle atrophy is a common outcome of many diseases, it is doubtful that a single gene or pathway initiates or mediates the breakdown of myofibrils. Interestingly, however, is the observation that upregulation of the E3 ligases, MuRF1 and MAFbx, is a common feature of many divergent atrophy conditions. The challenge for the field of muscle biology is to understand how all of the various molecules, transcription factors, and signaling pathways interact to produce muscle atrophy and to identify the critical factors for intervention.

scholarly journals Dietary supplementation with shiikuwasha extract attenuates dexamethasone-induced skeletal muscle atrophy in aged rats

SpringerPlus ◽  
2016 ◽  
Vol 5 (1) ◽  
Author(s):  
Yasuyuki Sakata ◽  
Tomoyuki Okamoto ◽  
Kazutaka Oshio ◽  
Hirohiko Nakamura ◽  
Hiroshi Iwamoto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Dietary Supplementation ◽  
Skeletal Muscle Atrophy ◽  
Aged Rats

Temporal alterations in protein signaling cascades during recovery from muscle atrophy

2003 ◽  
Vol 285 (2) ◽  
pp. C391-C398 ◽  
Author(s):  
Thomas E. Childs ◽  
Espen E. Spangenburg ◽  
Dharmesh R. Vyas ◽  
Frank W. Booth
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Atrophy ◽  
Soleus Muscle ◽  
Time Course ◽  
Glycogen Synthase ◽  
Early Time ◽  
Protein Translation ◽  
Skeletal Muscle Atrophy ◽  
Time Points

Currently, the repertoire of cellular and molecular pathways that control skeletal muscle atrophy and hypertrophy are not well defined. It is possible that intracellular regulatory signaling pathways are active at different times during the muscle hypertrophy process. The hypothesis of the given experiments was that cellular signals related to protein translation would be active at early time points of skeletal muscle regrowth, whereas transcriptional signals would be active at later time points of skeletal muscle regrowth. The phosphorylation status of p38 MAPK and JNK increased at the end of limb immobilization but returned to control values at recovery day 3. Transient increases in phosphorylation and in protein concentration occurred during recovery of soleus muscle mass. Phosphorylation of Akt, p70S6k, and signal transducer and activator of transcription 3 (STAT3) peaked on recovery day 3 compared with day 0. Glycogen synthase kinase (GSK)-3β phosphorylation was increased on the sixth and fifteenth recovery day. In addition, transient peaks in seven protein concentrations occurred at different times of recovery: STAT3, calcineurin A (CaNA), CaNB, and β4E-BP1 protein concentrations peaked on the third recovery day; p70S6k, STAT3, Akt, and GSK3-β peaked on the sixth recovery day; and GSK3-β peaked on the fifteenth recovery day. The apexes of STAT3 and GSK3-β protein concentrations remained elevated for two recovery time points. Thus the time course of increase in molecules of signaling pathways differed as the young rat soleus muscle regrew from an atrophied state.

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