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Musculoskeletal Aging and Sarcopenia in the Elderly

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 39803

Special Issue Editor

Special Issue Information

Dear Colleagues,

The loss of skeletal muscle mass and strength/function, referred to as sarcopenia, is a pervasive feature of aging. The remarkable prevalence of sarcopenia and its association with a broad range of negative health-related outcomes have instigated a great deal of research on the pathophysiology of muscle aging. This has led to the identification of several biological pathways that may be exploited for biomarker discovery and/or therapeutic purposes. This Special Issue aims at convening basic and clinical researchers working in the area of sarcopenia to foster our understanding of the molecular determinants of muscle aging and their modulation by specific interventions.

I therefore invite you to submit your latest original research or review articles on muscle aging and sarcopenia to this Special Issue. Priority will be given to articles proposing translational geroscience approaches as well as to those using multi-marker strategies and omics platforms for the study of sarcopenia.

Prof. Emanuele Marzetti
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Biological pillars of aging
  • Biogerontology
  • Biomarkers
  • Drug discovery
  • Exercise
  • Geroscience
  • Multi-marker
  • Nutrition
  • Omics
  • Precision medicine

Published Papers (8 papers)

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Editorial

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3 pages, 193 KiB  
Editorial
Musculoskeletal Aging and Sarcopenia in the Elderly
by Emanuele Marzetti
Int. J. Mol. Sci. 2022, 23(5), 2808; https://doi.org/10.3390/ijms23052808 - 04 Mar 2022
Cited by 5 | Viewed by 3034
Abstract
The loss of skeletal muscle mass and strength/function, referred to as sarcopenia, is a pervasive feature of aging [...] Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)

Research

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20 pages, 1587 KiB  
Article
A Plasma Proteomic Signature of Skeletal Muscle Mitochondrial Function
by Marta Zampino, Toshiko Tanaka, Ceereena Ubaida-Mohien, Giovanna Fantoni, Julián Candia, Richard D. Semba and Luigi Ferrucci
Int. J. Mol. Sci. 2020, 21(24), 9540; https://doi.org/10.3390/ijms21249540 - 15 Dec 2020
Cited by 10 | Viewed by 2633
Abstract
Although mitochondrial dysfunction has been implicated in aging, physical function decline, and several age-related diseases, an accessible and affordable measure of mitochondrial health is still lacking. In this study we identified the proteomic signature of muscular mitochondrial oxidative capacity in plasma. In 165 [...] Read more.
Although mitochondrial dysfunction has been implicated in aging, physical function decline, and several age-related diseases, an accessible and affordable measure of mitochondrial health is still lacking. In this study we identified the proteomic signature of muscular mitochondrial oxidative capacity in plasma. In 165 adults, we analyzed the association between concentrations of plasma proteins, measured using the SOMAscan assay, and skeletal muscle maximal oxidative phosphorylation capacity assessed as post-exercise phosphocreatine recovery time constant (τPCr) by phosphorous magnetic resonance spectroscopy. Out of 1301 proteins analyzed, we identified 87 proteins significantly associated with τPCr, adjusting for age, sex, and phosphocreatine depletion. Sixty proteins were positively correlated with better oxidative capacity, while 27 proteins were correlated with poorer capacity. Specific clusters of plasma proteins were enriched in the following pathways: homeostasis of energy metabolism, proteostasis, response to oxidative stress, and inflammation. The generalizability of these findings would benefit from replication in an independent cohort and in longitudinal analyses. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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16 pages, 1959 KiB  
Article
Taurine Attenuates Catabolic Processes Related to the Onset of Sarcopenia
by Alessandra Barbiera, Silvia Sorrentino, Elisa Lepore, Andrea Carfì, Gigliola Sica, Gabriella Dobrowolny and Bianca Maria Scicchitano
Int. J. Mol. Sci. 2020, 21(22), 8865; https://doi.org/10.3390/ijms21228865 - 23 Nov 2020
Cited by 12 | Viewed by 3659
Abstract
Sarcopenia that occurs with advancing age is characterized by a gradual loss of muscle protein component due to the activation of catabolic pathways, increased level of inflammation, and mitochondrial dysfunction. Experimental evidence demonstrates that several physio-pathological processes involved in the onset of sarcopenia [...] Read more.
Sarcopenia that occurs with advancing age is characterized by a gradual loss of muscle protein component due to the activation of catabolic pathways, increased level of inflammation, and mitochondrial dysfunction. Experimental evidence demonstrates that several physio-pathological processes involved in the onset of sarcopenia may be counteracted by the intake of specific amino acids or antioxidant molecules, suggesting that diet may represent an effective strategy for improving the anabolic response of muscle during aging. The non-essential amino acid taurine is highly expressed in several mammalian tissues, including skeletal muscle where it is involved in the ion channel regulation, in the modulation of intracellular calcium concentration, and where it plays an important role as an antioxidant and anti-inflammatory factor. Here, with the purpose to reproduce the chronic low-grade inflammation characteristics of senescent muscle in an in vitro system, we exploited the role of Tumor Necrosis Factor α (TNF) and we analyzed the effect of taurine in the modulation of different signaling pathways known to be dysregulated in sarcopenia. We demonstrated that the administration of high levels of taurine in myogenic L6 cells stimulates the differentiation process by downregulating the expression of molecules involved in inflammatory pathways and modulating processes such as autophagy and apoptosis. Although further studies are currently ongoing in our laboratory to better elucidate the molecular mechanisms responsible for the positive effect of taurine on myogenic differentiation, this study suggests that taurine supplementation may represent a strategy to delay the loss of mass and functionality characteristic of senescent muscles. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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Review

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25 pages, 2004 KiB  
Review
Improper Remodeling of Organelles Deputed to Ca2+ Handling and Aerobic ATP Production Underlies Muscle Dysfunction in Ageing
by Feliciano Protasi, Laura Pietrangelo and Simona Boncompagni
Int. J. Mol. Sci. 2021, 22(12), 6195; https://doi.org/10.3390/ijms22126195 - 08 Jun 2021
Cited by 11 | Viewed by 5994
Abstract
Proper skeletal muscle function is controlled by intracellular Ca2+ concentration and by efficient production of energy (ATP), which, in turn, depend on: (a) the release and re-uptake of Ca2+ from sarcoplasmic-reticulum (SR) during excitation–contraction (EC) coupling, which controls the contraction and [...] Read more.
Proper skeletal muscle function is controlled by intracellular Ca2+ concentration and by efficient production of energy (ATP), which, in turn, depend on: (a) the release and re-uptake of Ca2+ from sarcoplasmic-reticulum (SR) during excitation–contraction (EC) coupling, which controls the contraction and relaxation of sarcomeres; (b) the uptake of Ca2+ into the mitochondrial matrix, which stimulates aerobic ATP production; and finally (c) the entry of Ca2+ from the extracellular space via store-operated Ca2+ entry (SOCE), a mechanism that is important to limit/delay muscle fatigue. Abnormalities in Ca2+ handling underlie many physio-pathological conditions, including dysfunction in ageing. The specific focus of this review is to discuss the importance of the proper architecture of organelles and membrane systems involved in the mechanisms introduced above for the correct skeletal muscle function. We reviewed the existing literature about EC coupling, mitochondrial Ca2+ uptake, SOCE and about the structural membranes and organelles deputed to those functions and finally, we summarized the data collected in different, but complementary, projects studying changes caused by denervation and ageing to the structure and positioning of those organelles: a. denervation of muscle fibers—an event that contributes, to some degree, to muscle loss in ageing (known as sarcopenia)—causes misplacement and damage: (i) of membrane structures involved in EC coupling (calcium release units, CRUs) and (ii) of the mitochondrial network; b. sedentary ageing causes partial disarray/damage of CRUs and of calcium entry units (CEUs, structures involved in SOCE) and loss/misplacement of mitochondria; c. functional electrical stimulation (FES) and regular exercise promote the rescue/maintenance of the proper architecture of CRUs, CEUs, and of mitochondria in both denervation and ageing. All these structural changes were accompanied by related functional changes, i.e., loss/decay in function caused by denervation and ageing, and improved function following FES or exercise. These data suggest that the integrity and proper disposition of intracellular organelles deputed to Ca2+ handling and aerobic generation of ATP is challenged by inactivity (or reduced activity); modifications in the architecture of these intracellular membrane systems may contribute to muscle dysfunction in ageing and sarcopenia. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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12 pages, 1251 KiB  
Review
How Can Malnutrition Affect Autophagy in Chronic Heart Failure? Focus and Perspectives
by Giovanni Corsetti, Evasio Pasini, Claudia Romano, Carol Chen-Scarabelli, Tiziano M. Scarabelli, Vincenzo Flati, Louis Saravolatz and Francesco S. Dioguardi
Int. J. Mol. Sci. 2021, 22(7), 3332; https://doi.org/10.3390/ijms22073332 - 24 Mar 2021
Cited by 17 | Viewed by 2991
Abstract
Chronic heart failure (CHF) is a disease with important clinical and socio-economic ramifications. Malnutrition and severe alteration of the protein components of the body (protein disarrangements), common conditions in CHF patients, are independent correlates of heart dysfunction, disease progression, and mortality. Autophagy, a [...] Read more.
Chronic heart failure (CHF) is a disease with important clinical and socio-economic ramifications. Malnutrition and severe alteration of the protein components of the body (protein disarrangements), common conditions in CHF patients, are independent correlates of heart dysfunction, disease progression, and mortality. Autophagy, a prominent occurrence in the heart of patients with advanced CHF, is a self-digestive process that prolongs myocardial cell lifespan by the removal of cytosolic components, such as aging organelles and proteins, and recycles the constituent elements for new protein synthesis. However, in specific conditions, excessive activation of autophagy can lead to the destruction of molecules and organelles essential to cell survival, ultimately leading to organ failure and patient death. In this review, we aim to describe the experimental and clinical evidence supporting a pathophysiological role of nutrition and autophagy in the progression of CHF. The understanding of the mechanisms underlying the interplay between nutrition and autophagy may have important clinical implications by providing molecular targets for innovative therapeutic strategies in CHF patients. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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17 pages, 1851 KiB  
Review
The Interplay between Mitochondrial Morphology and Myomitokines in Aging Sarcopenia
by Vanina Romanello
Int. J. Mol. Sci. 2021, 22(1), 91; https://doi.org/10.3390/ijms22010091 - 23 Dec 2020
Cited by 43 | Viewed by 5420
Abstract
Sarcopenia is a chronic disease characterized by the progressive loss of skeletal muscle mass, force, and function during aging. It is an emerging public problem associated with poor quality of life, disability, frailty, and high mortality. A decline in mitochondria quality control pathways [...] Read more.
Sarcopenia is a chronic disease characterized by the progressive loss of skeletal muscle mass, force, and function during aging. It is an emerging public problem associated with poor quality of life, disability, frailty, and high mortality. A decline in mitochondria quality control pathways constitutes a major mechanism driving aging sarcopenia, causing abnormal organelle accumulation over a lifetime. The resulting mitochondrial dysfunction in sarcopenic muscles feedbacks systemically by releasing the myomitokines fibroblast growth factor 21 (FGF21) and growth and differentiation factor 15 (GDF15), influencing the whole-body homeostasis and dictating healthy or unhealthy aging. This review describes the principal pathways controlling mitochondrial quality, many of which are potential therapeutic targets against muscle aging, and the connection between mitochondrial dysfunction and the myomitokines FGF21 and GDF15 in the pathogenesis of aging sarcopenia. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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15 pages, 1442 KiB  
Review
Physical Exercise and Myokines: Relationships with Sarcopenia and Cardiovascular Complications
by Sandra Maria Barbalho, Uri Adrian Prync Flato, Ricardo José Tofano, Ricardo de Alvares Goulart, Elen Landgraf Guiguer, Cláudia Rucco P. Detregiachi, Daniela Vieira Buchaim, Adriano Cressoni Araújo, Rogério Leone Buchaim, Fábio Tadeu Rodrigues Reina, Piero Biteli, Daniela O. B. Rodrigues Reina and Marcelo Dib Bechara
Int. J. Mol. Sci. 2020, 21(10), 3607; https://doi.org/10.3390/ijms21103607 - 20 May 2020
Cited by 76 | Viewed by 10298
Abstract
Skeletal muscle is capable of secreting different factors in order to communicate with other tissues. These mediators, the myokines, show potentially far-reaching effects on non-muscle tissues and can provide a molecular interaction between muscle and body physiology. Sarcopenia is a chronic degenerative neuromuscular [...] Read more.
Skeletal muscle is capable of secreting different factors in order to communicate with other tissues. These mediators, the myokines, show potentially far-reaching effects on non-muscle tissues and can provide a molecular interaction between muscle and body physiology. Sarcopenia is a chronic degenerative neuromuscular disease closely related to cardiomyopathy and chronic heart failure, which influences the production and release of myokines. Our objective was to explore the relationship between myokines, sarcopenia, and cardiovascular diseases (CVD). The autocrine, paracrine, and endocrine actions of myokines include regulation of energy expenditure, insulin sensitivity, lipolysis, free fatty acid oxidation, adipocyte browning, glycogenolysis, glycogenesis, and general metabolism. A sedentary lifestyle accelerates the aging process and is a risk factor for developing sarcopenia, metabolic syndrome, and CVD. Increased adipose tissue resulting from the decrease in muscle mass in patients with sarcopenia may also be involved in the pathology of CVD. Myokines are protagonists in the complex condition of sarcopenia, which is associated with adverse clinical outcomes in patients with CVD. The discovery of new pathways and the link between myokines and CVD remain a cornerstone toward multifaceted interventions and perhaps the minimization of the damage resulting from muscle loss induced by factors such as atherosclerosis. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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12 pages, 634 KiB  
Review
Re-Setting the Circadian Clock Using Exercise against Sarcopenia
by Youngju Choi, Jinkyung Cho, Mi-Hyun No, Jun-Won Heo, Eun-Jeong Cho, Eunwook Chang, Dong-Ho Park, Ju-Hee Kang and Hyo-Bum Kwak
Int. J. Mol. Sci. 2020, 21(9), 3106; https://doi.org/10.3390/ijms21093106 - 28 Apr 2020
Cited by 26 | Viewed by 5219
Abstract
Sarcopenia is defined as the involuntary loss of skeletal muscle mass and function with aging and is associated with several adverse health outcomes. Recently, the disruption of regular circadian rhythms, due to shift work or nocturnal lifestyle, is emerging as a novel deleterious [...] Read more.
Sarcopenia is defined as the involuntary loss of skeletal muscle mass and function with aging and is associated with several adverse health outcomes. Recently, the disruption of regular circadian rhythms, due to shift work or nocturnal lifestyle, is emerging as a novel deleterious factor for the development of sarcopenia. The underlying mechanisms responsible for circadian disruption-induced sarcopenia include molecular circadian clock and mitochondrial function associated with the regulation of circadian rhythms. Exercise is a potent modulator of skeletal muscle metabolism and is considered to be a crucial preventative and therapeutic intervention strategy for sarcopenia. Moreover, emerging evidence shows that exercise, acting as a zeitgeber (time cue) of the skeletal muscle clock, can be an efficacious tool for re-setting the clock in sarcopenia. In this review, we provide the evidence of the impact of circadian disruption on skeletal muscle loss resulting in sarcopenia. Furthermore, we highlight the importance of exercise timing (i.e., scheduled physical activity) as a novel therapeutic strategy to target circadian disruption in skeletal muscle. Full article
(This article belongs to the Special Issue Musculoskeletal Aging and Sarcopenia in the Elderly)
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