Mitochondrial dysfunction and sarcopenia of aging: From signaling pathways to clinical trials

Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on th...

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Vydáno v:	The international journal of biochemistry & cell biology Ročník 45; číslo 10; s. 2288 - 2301
Hlavní autoři:	Marzetti, Emanuele, Calvani, Riccardo, Cesari, Matteo, Buford, Thomas W., Lorenzi, Maria, Behnke, Bradley J., Leeuwenburgh, Christiaan
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Netherlands Elsevier Ltd 01.10.2013
Témata:	Aged Aging - metabolism Aging - pathology Animals Apoptosis Apoptosis - physiology biochemistry Biomarkers clinical trials Fusion and fission health care workers Humans inflammation lifestyle Mitochondria - metabolism Mitochondria - pathology Mitophagy Mitophagy - physiology monitoring muscles myotubes oxidative stress Oxidative Stress - physiology pathogenesis pathophysiology Randomized Controlled Trials as Topic - methods sarcopenia Sarcopenia - metabolism Sarcopenia - pathology Sarcopenia - therapy Signal Transduction society Vascular dysfunction Bcl-2 Fusion and fission eNOS RCT mtDNA OXPHOS Vascular dysfunction Atg protein EndoG Mitophagy Drp1 CSA IFM NF-κB Mfn LAMP-2 SDH MFRTA iNOS UPS AngII LC3 AIF MQC 31P-NMR Fis1 GH VDR IGF-1 PGC-1α SSM COX TA OMM NOS TNF-α ETC VL nNOS ROS Biomarkers TFAM FoxO3 COPD Apoptosis nuclear factor κB outer mitochondrial membrane insulin-like growth factor-1 P-NMR Forkhead box O3 cytochrome c oxidase fission protein 1 mitochondrial quality control endothelial nitric oxide synthase vitamin D receptor nitric oxide synthase autophagy-related protein B-cell leukemia-2 vastus lateralis dynamin-related protein 1 ubiquitin–proteasome system oxidative phosphorylation endonuclease G angiotensin II subsarcolemmal mitochondria cross-sectional area P nuclear magnetic resonance tibialis anterior inducible nitric oxide synthase microtubule-associated protein 1 light chain 3 lysosomal-associated membrane protein 2 reactive oxygen species mitochondrial transcription factor A growth hormone electron transport chain mitochondrial free radical theory of aging mitochondrial DNA neuronal nitric oxide synthase peroxisome proliferator-activated receptor-γ coactivator-1α randomized controlled trial succinate dehydrogenase tumor-necrosis factor α apoptosis-inducing factor mitofusin chronic obstructive pulmonary disease interfibrillar mitochondria
ISSN:	1357-2725, 1878-5875, 1878-5875
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Abstract	Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes – including oxidative stress, quality control mechanisms and apoptotic signaling – on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
AbstractList	Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes – including oxidative stress, quality control mechanisms and apoptotic signaling – on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes – including oxidative stress, quality control mechanisms and apoptotic signaling – on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes – including oxidative stress, quality control mechanisms and apoptotic signaling – on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
Author	Calvani, Riccardo Leeuwenburgh, Christiaan Buford, Thomas W. Behnke, Bradley J. Lorenzi, Maria Cesari, Matteo Marzetti, Emanuele
AuthorAffiliation	d Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA e Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA b Institute of Crystallography, Italian National Research Council (CNR), Bari 70126, Italy c Institut du Vieillissement, Gérontopôle and INSERM Unit 1027, University of Toulouse, Toulouse 31000, France a Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy
AuthorAffiliation_xml	– name: a Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy – name: d Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA – name: e Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA – name: c Institut du Vieillissement, Gérontopôle and INSERM Unit 1027, University of Toulouse, Toulouse 31000, France – name: b Institute of Crystallography, Italian National Research Council (CNR), Bari 70126, Italy
Author_xml	– sequence: 1 givenname: Emanuele surname: Marzetti fullname: Marzetti, Emanuele email: emarzetti@live.com organization: Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy – sequence: 2 givenname: Riccardo surname: Calvani fullname: Calvani, Riccardo organization: Institute of Crystallography, Italian National Research Council (CNR), Bari 70126, Italy – sequence: 3 givenname: Matteo surname: Cesari fullname: Cesari, Matteo organization: Institut du Vieillissement, Gérontopôle and INSERM Unit 1027, University of Toulouse, Toulouse 31000, France – sequence: 4 givenname: Thomas W. surname: Buford fullname: Buford, Thomas W. organization: Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA – sequence: 5 givenname: Maria surname: Lorenzi fullname: Lorenzi, Maria organization: Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy – sequence: 6 givenname: Bradley J. surname: Behnke fullname: Behnke, Bradley J. organization: Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA – sequence: 7 givenname: Christiaan surname: Leeuwenburgh fullname: Leeuwenburgh, Christiaan organization: Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/23845738$$D View this record in MEDLINE/PubMed
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Snippet	Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and...
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SubjectTerms	Aged Aging - metabolism Aging - pathology Animals Apoptosis Apoptosis - physiology biochemistry Biomarkers clinical trials Fusion and fission health care workers Humans inflammation lifestyle Mitochondria - metabolism Mitochondria - pathology Mitophagy Mitophagy - physiology monitoring muscles myotubes oxidative stress Oxidative Stress - physiology pathogenesis pathophysiology Randomized Controlled Trials as Topic - methods sarcopenia Sarcopenia - metabolism Sarcopenia - pathology Sarcopenia - therapy Signal Transduction society Vascular dysfunction
Title	Mitochondrial dysfunction and sarcopenia of aging: From signaling pathways to clinical trials
URI	https://dx.doi.org/10.1016/j.biocel.2013.06.024 https://www.ncbi.nlm.nih.gov/pubmed/23845738 https://www.proquest.com/docview/1429642790 https://www.proquest.com/docview/1803093538 https://pubmed.ncbi.nlm.nih.gov/PMC3759621
Volume	45
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