New Molecular Targets and Lifestyle Interventions to Delay Aging Sarcopenia

Sanchís-Gomar, Fabián; Pareja‐Galeano, Helios; Mayero, Sara; Pérez-Quilis, Carme; Lucía, Alejandro

doi:10.3389/fnagi.2014.00156

Cited by 21 publications

(20 citation statements)

References 43 publications

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“…A major problem of demographic ageing is sarcopenia, i.e., age-related loss of muscle mass leading to functional impairment. Although pharmacologic approaches have been proposed to combat sarcopenia, these are not without potential risks and secondary effects (Sanchis-Gomar et al, 2014). The latter is linked to falls, disability, dependence, hospitalization, and mortality, generating considerable healthcare, and social costs (Landi et al, 2012;Mohler et al, 2014).…”

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confidence: 99%

“…The latter is linked to falls, disability, dependence, hospitalization, and mortality, generating considerable healthcare, and social costs (Landi et al, 2012;Mohler et al, 2014). Although pharmacologic approaches have been proposed to combat sarcopenia, these are not without potential risks and secondary effects (Sanchis-Gomar et al, 2014). A potential alternative is regenerative medicine, whose goal is tissue repair/substitution with transplanted healthy tissue, e.g., embryonic stem (ES) cells from the same individual or a compatible donor.…”

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confidence: 99%

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IPSCs, a Promising Tool to Restore Muscle Atrophy

Pareja‐Galeano

Sanchís-Gomar

Emanuele³

et al. 2015

Journal Cellular Physiology

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Induced pluripotent stem cells (iPSCs) are a promising tool for regenerative medicine in chronic conditions associated with muscle atrophy since iPSCs are easier to obtain, pose less ethical limitations and can better capture human genetic diversity compared with human embryonic stem cells. We highlight the potentiality of iPSCs for treating muscle‐affecting conditions for which no effective cure is yet available, notably aging sarcopenia and inherited neurometabolic conditions. J. Cell. Physiol. 231: 259–260, 2016. © 2015 Wiley Periodicals, Inc.

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confidence: 99%

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confidence: 99%

IPSCs, a Promising Tool to Restore Muscle Atrophy

Pareja‐Galeano

Sanchís-Gomar

Emanuele³

et al. 2015

Journal Cellular Physiology

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“…Resistance training also can increase circulating irisin [67] and improve cognitive performance [62]. In addition, physical exercise and caloric restriction can benefit age-related insulin resistance, reduced mitochondrial biogenesis, and failure of autophagy [68]. However, it is undesirable to use caloric restriction alone in sarcopenic elderly, which results in further loss of lean tissue mass.…”

Section: From Sarcopenia To Frailty: the Potential Target Molecules Omentioning

confidence: 99%

“…A number of aging-associated molecular signals might be the potential target in the prevention and treatment of sarcopenia, frailty, and cognitive impairment. Genetic or pharmacological regulation of NAD+/Sirt1, sestrins/AMPK/PGC1α, IGF-1/Akt/mTOR, TGF-β, myostatin, activins, GDFs /SMAD2/3, BMPs/SMAD1/5/8 signal molecules, myokine irisin and FGF21, the antagonist of myokine myostatin propeptide follistatin or follistatin-like 3, and urocortins can not only improve muscle mass and/or function but also delay frailty and agerelated diseases [31,54,68]. Besides dietary restriction and exercise, geroscience interventions with translational potential include mTOR inhibitors, metformin and acarbose, NAD precursors and sirtuin activators, modifiers of senescence and telomere dysfunction, hormonal and circulating factors, and mitochondrial-targeted therapeutics [78].…”

Section: From Sarcopenia To Frailty: the Potential Target Molecules Omentioning

confidence: 99%

From Sarcopenia to Frailty: The Pathophysiological Basis and Potential Target Molecules of Intervention

Yu¹,

Ruan²,

Greco³

2017

Frailty and Sarcopenia - Onset, Development and Clinical Challenges

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Skeletal muscle is not only an endocrine organ but also one of core components of muscloskeletal system. Sarcopenia refers to a decline in the skeletal muscle mass and function. The former involves the size and number of changes in two types of myofibers, lower satellite cell density, and regeneration ability. The latter shows a loss of muscle strength. Frailty is a geriatric syndrome with multisystem impairment associated with increased vulnerability to stressors. Sarcopenia increases the risk of frailty and may be one of the major causes of physical frailty phenotype. Sarcopenia is also potentially associated with cognitive frailty phenotype. Aging might be the common underlying pathophysiology of sarcopenia and frailty. Therefore, there are some potential target molecules in aging-related signaling pathways that might be associated with sarcopenia and frailty. Nevertheless, sarcopenia can mediate metabolism and promote accelerate systemic aging, frailty, and age-related diseases by myokines in an endocrine manner. Lifestyle interventions (resistance exercise and dietary restriction) of gerontoscience are effective in the prevention of sarcopenia. Some pharmacological agents are registered in different phases of clinical trials for sarcopenia intervention. Phytochemicals, mTOR inhibitors, metformin and acarbose, NAD precursors, and sirtuin activators demonstrated that multiple target antiaging effects might also have preventive and therapeutic perspectives on sarcopenia and frailty.

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“…Other well-known hemodynamic, immunomodulatory and antiatherosclerotic effects of regular exercise are convincingly able to explain the epidemiologic data showed in this review. But nevertheless, molecules such as myostatin, FGF21 (150,151), apelin, and FSTL1 (152), to name just a few, are promising therapeutic agent of absolute interest. We are expecting ad hoc trials clarifying their real potential.…”

Section: Conclusive Remarksmentioning

confidence: 99%

New insights about the putative role of myokines in the context of cardiac rehabilitation and secondary cardiovascular prevention

et al. 2017

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Exercise training prevents the onset and the development of many chronic diseases, acting as an effective tool both for primary and for secondary prevention. Various mechanisms that may be the effectors of these beneficial effects have been proposed during the past decades: some of these are well recognized, others less. Muscular myokines, released during and after muscular contraction, have been proposed as key mediators of the systemic effects of the exercise. Nevertheless the availability of an impressive amount of evidence regarding the systemic effects of muscle-derived factors, few studies have examined key issues: (I) if skeletal muscle cells themselves are the main source of cytokine during exercise; (II) if the release of myokines into the systemic circulation reach an adequate concentration to provide significant effects in tissues far from skeletal muscle; (III) what may be the role carried out by muscular cytokine regarding the well-known benefits induced by regular exercise, first of all the anti-inflammatory effect of exercise. Furthermore, a greater part of our knowledge regarding myokines derives from the muscle of healthy subjects. This knowledge may not necessarily be transferred per se to subjects with chronic diseases implicating a direct or indirect muscular dysfunction and/or a chronic state of inflammation with persistent immune-inflammatory activation (and therefore increased circulating levels of some cytokines): cachexia, sarcopenia due to multiple factors, disability caused by neurological damage, chronic congestive heart failure (CHF) or coronary artery disease (CAD). A key point of future studies is to ascertain how is modified the muscular release of myokines in different categories of unhealthy subjects, both at baseline and after rehabilitation. The purpose of this review is to discuss the main findings on the role of myokines as putative mediators of the therapeutic benefits obtained through regular exercise in the context of secondary cardiovascular prevention.

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New Molecular Targets and Lifestyle Interventions to Delay Aging Sarcopenia

Cited by 21 publications

References 43 publications

IPSCs, a Promising Tool to Restore Muscle Atrophy

IPSCs, a Promising Tool to Restore Muscle Atrophy

From Sarcopenia to Frailty: The Pathophysiological Basis and Potential Target Molecules of Intervention

New insights about the putative role of myokines in the context of cardiac rehabilitation and secondary cardiovascular prevention

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