scholarly journals Regulation of microRNAs in Satellite Cell Renewal, Muscle Function, Sarcopenia and the Role of Exercise

2020 ◽  
Vol 21 (18) ◽  
pp. 6732 ◽  
Author(s):  
Stefania Fochi ◽  
Gaia Giuriato ◽  
Tonia De Simone ◽  
Macarena Gomez-Lira ◽  
Stefano Tamburin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Elderly ◽  
Cell Renewal ◽  
Muscle Adaptation ◽  
Muscle Plasticity ◽  
Skeletal Mass ◽  
General Aspects

Sarcopenia refers to a condition of progressive loss of skeletal muscle mass and function associated with a higher risk of falls and fractures in older adults. Musculoskeletal aging leads to reduced muscle mass and strength, affecting the quality of life in elderly people. In recent years, several studies contributed to improve the knowledge of the pathophysiological alterations that lead to skeletal muscle dysfunction; however, the molecular mechanisms underlying sarcopenia are still not fully understood. Muscle development and homeostasis require a fine gene expression modulation by mechanisms in which microRNAs (miRNAs) play a crucial role. miRNAs modulate key steps of skeletal myogenesis including satellite cells renewal, skeletal muscle plasticity, and regeneration. Here, we provide an overview of the general aspects of muscle regeneration and miRNAs role in skeletal mass homeostasis and plasticity with a special interest in their expression in sarcopenia and skeletal muscle adaptation to exercise in the elderly.

scholarly journals p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Barbé ◽  
Audrey Loumaye ◽  
Pascale Lause ◽  
Olli Ritvos ◽  
Jean-Paul Thissen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Body ◽  
Negative Regulator ◽  
Skeletal Muscle Hypertrophy ◽  
Myostatin Inhibition

Skeletal muscle, the most abundant tissue in the body, plays vital roles in locomotion and metabolism. Understanding the cellular processes that govern regulation of muscle mass and function represents an essential step in the development of therapeutic strategies for muscular disorders. Myostatin, a member of the TGF-β family, has been identified as a negative regulator of muscle development. Indeed, its inhibition induces an extensive skeletal muscle hypertrophy requiring the activation of Smad 1/5/8 and the Insulin/IGF-I signaling pathway, but whether other molecular mechanisms are involved in this process remains to be determined. Using transcriptomic data from various Myostatin inhibition models, we identified Pak1 as a potential mediator of Myostatin action on skeletal muscle mass. Our results show that muscle PAK1 levels are systematically increased in response to Myostatin inhibition, parallel to skeletal muscle mass, regardless of the Myostatin inhibition model. Using Pak1 knockout mice, we investigated the role of Pak1 in the skeletal muscle hypertrophy induced by different approaches of Myostatin inhibition. Our findings show that Pak1 deletion does not impede the skeletal muscle hypertrophy magnitude in response to Myostatin inhibition. Therefore, Pak1 is permissive for the skeletal muscle mass increase caused by Myostatin inhibition.

scholarly journals cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration

2012 ◽  
Vol 303 (1) ◽  
pp. E1-E17 ◽  
Author(s):  
Rebecca Berdeaux ◽  
Randi Stewart
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
Camp Signaling ◽  
Metabolic Phenotype ◽  
Muscle Adaptation ◽  
Age Related ◽  
Organ Systems

Among organ systems, skeletal muscle is perhaps the most structurally specialized. The remarkable subcellular architecture of this tissue allows it to empower movement with instructions from motor neurons. Despite this high degree of specialization, skeletal muscle also has intrinsic signaling mechanisms that allow adaptation to long-term changes in demand and regeneration after acute damage. The second messenger adenosine 3′,5′-monophosphate (cAMP) not only elicits acute changes within myofibers during exercise but also contributes to myofiber size and metabolic phenotype in the long term. Strikingly, sustained activation of cAMP signaling leads to pronounced hypertrophic responses in skeletal myofibers through largely elusive molecular mechanisms. These pathways can promote hypertrophy and combat atrophy in animal models of disorders including muscular dystrophy, age-related atrophy, denervation injury, disuse atrophy, cancer cachexia, and sepsis. cAMP also participates in muscle development and regeneration mediated by muscle precursor cells; thus, downstream signaling pathways may potentially be harnessed to promote muscle regeneration in patients with acute damage or muscular dystrophy. In this review, we summarize studies implicating cAMP signaling in skeletal muscle adaptation. We also highlight ligands that induce cAMP signaling and downstream effectors that are promising pharmacological targets.

scholarly journals ACTN3 genotype influences skeletal muscle mass regulation and response to dexamethasone

2020 ◽  
Author(s):  
J.T. Seto ◽  
K.N. Roeszler ◽  
L.R. Meehan ◽  
H.D. Wood ◽  
C. Tiong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Development ◽  
Muscle Wasting ◽  
The Elderly ◽  
Power Performance ◽  
Increased Risk ◽  
Disease Modifier ◽  
The Common ◽  
Anti Inflammatory

AbstractHomozygosity for the common ACTN3 null polymorphism (ACTN3 577X) results in α-actinin-3 deficiency in ~20% of humans worldwide and is linked to reduced sprint and power performance in both elite athletes and the general population. α-Actinin-3 deficiency is also associated with reduced muscle mass and strength, increased risk of sarcopenia in the elderly, and altered response to muscle wasting induced by denervation and immobilisation. ACTN3 genotype is also a disease modifier for Duchenne muscular dystrophy (DMD), with α-actinin-3 deficiency associated with slower disease progression. Here we show that α-actinin-3 plays a key role in the regulation of protein synthesis and breakdown signalling in skeletal muscle, and its influence on muscle mass begins during early postnatal muscle development. Actn3 genotype also influences the skeletal muscle response to the glucocorticoid dexamethasone. Following acute dexamethasone exposure, transcriptomic analyses by RT-qPCR and RNA-sequencing show reduced atrophy signalling (Mstn, Tmem100, mRas, Fbxo32, Trim63) and anti-inflammatory response in α-actinin-3 deficient mice compared to wild-type. α-Actinin-3 deficiency also protects against muscle wasting following prolonged daily treatment with dexamethasone in female, but not male mice. In combination, these data suggest that ACTN3 R577X is a pharmacogenetic variant influencing the anti-inflammatory and muscle wasting response to glucocorticoid therapy.

Abstract P377: Insulin, Muscle Mass and Exercise Performance in Overweight Women

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Benjamin Leon ◽  
Andrea Carnie ◽  
Shannon Jenkins ◽  
Kevin Smith ◽  
Gloria Zalos ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Upper Extremity ◽  
Muscle Mass ◽  
Fat Mass ◽  
Lean Mass ◽  
Exercise Performance ◽  
Plasma Insulin ◽  
Fasting Insulin ◽  
Load Bearing ◽  
Skeletal Mass

Introduction Obesity is associated with many negative health impacts, including hyperinsulinemia and reduced exercise performance, despite being associated with greater lean skeletal mass which works as the insulin-targeting and exercising organ. Purpose of Study We delineated the associations amongst cardiorespiratory capacity, fat mass, skeletal mass distributions, and fasting plasma insulin in overweight, non-diabetic women. Methods One hundred and seventy-two sedentary women, age 22 to 68 years (range), body mass index (BMI) (34.2 ± 6.3 [mean ± SD]; range 25.3 to 57.6 kg/m 2 ), underwent dual energy x-ray absorptiometry for body composition, fasting insulin, and graded treadmill exercise test using the Bruce protocol with measurement of oxygen consumption (peak VO 2 ). Results After adjustment for age, fasting insulin (9.8 ± 8.1; range 1.9 to 47.6 mcU/ml) was positively associated with BMI (r = 0.43, p<0.001), fat mass (r = 0.41, p< 0.001), load-bearing skeletal muscle mass (lower extremity lean mass; r = 0.29, p< 0.001), and non-load-bearing skeletal muscle mass (upper extremity lean mass; Figure, Panel A). By multiple regression analysis with age, fat mass and lower and upper extremity lean masses as covariates, fat mass, age and upper extremity lean mass (Figure, Panel B) were independent negative predictors of peak VO 2 (all p< 0.01). Lower extremity, however, trended to be positively predictive of peak VO 2 (p = 0.067). Conclusions In non-load-bearing muscle, increased lean mass associated with elevated plasma insulin is predictive of reduced oxygen consumption during exercise, suggesting additional load that may diminish cardiorespiratory exercise performance or intrinsic impairment in skeletal muscle function. In load-bearing muscle, compensatory hypertrophy due to increased fat and lean mass loads may preserve exercise performance.

scholarly journals Altered miRNA and mRNA Expression in Sika Deer Skeletal Muscle with Age

Genes ◽  
2020 ◽  
Vol 11 (2) ◽  
pp. 172
Author(s):  
Boyin Jia ◽  
Yuan Liu ◽  
Qining Li ◽  
Jiali Zhang ◽  
Chenxia Ge ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth And Development ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
Sika Deer ◽  
De Novo ◽  
Expression Profiles ◽  
Differentially Expressed ◽  
Growth Development ◽  
Development And Aging

Studies of the gene and miRNA expression profiles associated with the postnatal late growth, development, and aging of skeletal muscle are lacking in sika deer. To understand the molecular mechanisms of the growth and development of sika deer skeletal muscle, we used de novo RNA sequencing (RNA-seq) and microRNA sequencing (miRNA-seq) analyses to determine the differentially expressed (DE) unigenes and miRNAs from skeletal muscle tissues at 1, 3, 5, and 10 years in sika deer. A total of 51,716 unigenes, 171 known miRNAs, and 60 novel miRNAs were identified based on four mRNA and small RNA libraries. A total of 2,044 unigenes and 11 miRNAs were differentially expressed between adolescence and juvenile sika deer, 1,946 unigenes and 4 miRNAs were differentially expressed between adult and adolescent sika deer, and 2,209 unigenes and 1 miRNAs were differentially expressed between aged and adult sika deer. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses showed that DE unigenes and miRNA were mainly related to energy and substance metabolism, processes that are closely associate with the growth, development, and aging of skeletal muscle. We also constructed mRNA–mRNA and miRNA–mRNA interaction networks related to the growth, development, and aging of skeletal muscle. The results show that mRNA (Myh1, Myh2, Myh7, ACTN3, etc.) and miRNAs (miR-133a, miR-133c, miR-192, miR-151-3p, etc.) may play important roles in muscle growth and development, and mRNA (WWP1, DEK, UCP3, FUS, etc.) and miRNAs (miR-17-5p, miR-378b, miR-199a-5p, miR-7, etc.) may have key roles in muscle aging. In this study, we determined the dynamic miRNA and unigenes transcriptome in muscle tissue for the first time in sika deer. The age-dependent miRNAs and unigenes identified will offer insights into the molecular mechanism underlying muscle development, growth, and maintenance and will also provide valuable information for sika deer genetic breeding.

scholarly journals Effects of PM2.5 on Skeletal Muscle Mass and Body Fat Mass of the Elderly in Taipei, Taiwan

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Chi-Hsien Chen ◽  
Li-Ying Huang ◽  
Kang-Yun Lee ◽  
Chih-Da Wu ◽  
Hung-Che Chiang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Body Fat ◽  
Fat Mass ◽  
Skeletal Muscle Mass ◽  
The Elderly ◽  
Body Fat Mass

scholarly journals MuRF1/TRIM63, Master Regulator of Muscle Mass

2020 ◽  
Vol 21 (18) ◽  
pp. 6663 ◽  
Author(s):  
Dulce Peris-Moreno ◽  
Daniel Taillandier ◽  
Cécile Polge
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Cardiac Functions ◽  
Important Player ◽  
Cardiac Muscles ◽  
Inhibitory Molecules

The E3 ubiquitin ligase MuRF1/TRIM63 was identified 20 years ago and suspected to play important roles during skeletal muscle atrophy. Since then, numerous studies have been conducted to decipher the roles, molecular mechanisms and regulation of this enzyme. This revealed that MuRF1 is an important player in the skeletal muscle atrophy process occurring during catabolic states, making MuRF1 a prime candidate for pharmacological treatments against muscle wasting. Indeed, muscle wasting is an associated event of several diseases (e.g., cancer, sepsis, diabetes, renal failure, etc.) and negatively impacts the prognosis of patients, which has stimulated the search for MuRF1 inhibitory molecules. However, studies on MuRF1 cardiac functions revealed that MuRF1 is also cardioprotective, revealing a yin and yang role of MuRF1, being detrimental in skeletal muscle and beneficial in the heart. This review discusses data obtained on MuRF1, both in skeletal and cardiac muscles, over the past 20 years, regarding the structure, the regulation, the location and the different functions identified, and the first inhibitors reported, and aim to draw the picture of what is known about MuRF1. The review also discusses important MuRF1 characteristics to consider for the design of future drugs to maintain skeletal muscle mass in patients with different pathologies.

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