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المؤلفون: Anna-Maria Joseph, David G. Levin, Bhanuprasad Sandesara, Todd M. Manini, David M. Gundermann, Peter J. Adhihetty, Christiaan Leeuwenburgh, Nicholas R. Wawrzyniak
المصدر: Oncotarget
مصطلحات موضوعية: musculoskeletal diseases, Male, 0301 basic medicine, Gerontology, SIRT3, Vastus lateralis muscle, NF-E2-Related Factor 1, PGC-1α, Physiology, Mitochondrion, medicine.disease_cause, Antioxidants, 03 medical and health sciences, Research Paper: Gerotarget (Focus on Aging), Sirtuin 3, Surveys and Questionnaires, medicine, Humans, skeletal muscle, Muscle, Skeletal, Aged, Fatigue Syndrome, Chronic, Kinesiology, Gerotarget, business.industry, Cytochromes c, Skeletal muscle, Chronic fatigue, social sciences, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Mitochondrial morphology, humanities, Mitochondria, Muscle, mitochondria, Oxidative Stress, 030104 developmental biology, medicine.anatomical_structure, Oncology, fatigue, Female, business, human activities, Oxidative stress, Signal Transduction
الوصف: // Nicholas R. Wawrzyniak 1 , Anna-Maria Joseph 2 , David G. Levin 1 , David M. Gundermann 2 , Christiaan Leeuwenburgh 2 , Bhanuprasad Sandesara 2 , Todd M. Manini 2 and Peter J. Adhihetty 1 1 Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA 2 Department of Aging and Geriatric Research, Division of Biology of Aging, University of Florida, Gainesville, Florida, USA Correspondence to: Peter J. Adhihetty, email: // Todd M. Manini, email: // Keywords : fatigue; skeletal muscle; mitochondria; PGC-1α; Gerotarget Received : January 11, 2016 Accepted : June 09, 2016 Published : July 18, 2016 Abstract Fatigue is a symptom of many diseases, but it can also manifest as a unique medical condition, such as idiopathic chronic fatigue (ICF). While the prevalence of ICF increases with age, mitochondrial content and function decline with age, which may contribute to ICF. The purpose of this study was to determine whether skeletal muscle mitochondrial dysregulation and oxidative stress is linked to ICF in older adults. Sedentary, old adults ( n = 48, age 72.4 ± 5.3 years) were categorized into ICF and non-fatigued (NF) groups based on the FACIT-Fatigue questionnaire. ICF individuals had a FACIT score one standard deviation below the mean for non-anemic adults > 65 years and were excluded according to CDC diagnostic criteria for ICF. Vastus lateralis muscle biopsies were analyzed, showing reductions in mitochondrial content and suppression of mitochondrial regulatory proteins Sirt3, PGC-1α, NRF-1, and cytochrome c in ICF compared to NF. Additionally, mitochondrial morphology proteins, antioxidant enzymes, and lipid peroxidation were unchanged in ICF individuals. Our data suggests older adults with ICF have reduced skeletal muscle mitochondrial content and biogenesis signaling that cannot be accounted for by increased oxidative damage.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::eae1054fd7d4a1da8402899aa746e203Test
https://doi.org/10.18632/oncotarget.10685Test -
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المؤلفون: Riccardo Calvani, Anna-Maria Joseph, Christiaan Leeuwenburgh, Roberto Bernabei, Maurizio Bossola, Alfredo Miccheli, Peter J. Adhihetty, Emanuele Marzetti
المصدر: Biological chemistry
394 (2013): 393–414. doi:10.1515/hsz-2012-0247
info:cnr-pdr/source/autori:Calvani R.; Joseph A.-M.; Adhihetty P.J.; Miccheli A.; Bossola M.; Leeuwenburgh C.; Bernabei R.; Marzetti E./titolo:Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy/doi:10.1515%2Fhsz-2012-0247/rivista:Biological chemistry (Print)/anno:2013/pagina_da:393/pagina_a:414/intervallo_pagine:393–414/volume:394مصطلحات موضوعية: autophagy, fusion, Sarcopenia, medicine.medical_specialty, Clinical Biochemistry, Cellular homeostasis, apoptosis, fission, mitophagy, oxidative stress, Mitochondrion, Biology, medicine.disease_cause, Biochemistry, Article, Internal medicine, Mitophagy, medicine, Humans, Molecular Biology, Atrophic, Settore MED/09 - MEDICINA INTERNA, Autophagy, medicine.disease, Muscular Disorders, Atrophic, Muscle atrophy, Mitochondria, Oxidative Stress, Muscular Disorders, Endocrinology, medicine.symptom, Signal transduction, Neuroscience, Oxidative stress, Signal Transduction
الوصف: Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7b2fe59e281294c13c3f58bd181d80e2Test
https://doi.org/10.1515/hsz-2012-0247Test -
3
المصدر: Sports Medicine. 33:783-793
مصطلحات موضوعية: Aging, medicine.medical_specialty, Mitochondrial DNA, Muscle Fibers, Skeletal, Physical Therapy, Sports Therapy and Rehabilitation, Physical exercise, Mitochondrion, Adenosine Triphosphate, Physical medicine and rehabilitation, Endurance training, medicine, Humans, Orthopedics and Sports Medicine, Exercise physiology, Exercise, business.industry, Muscles, Skeletal muscle, DNA, Mitochondria, medicine.anatomical_structure, Mitochondrial biogenesis, Physical Endurance, Calcium, medicine.symptom, business, Neuroscience, Signal Transduction, Muscle contraction
الوصف: Behavioural and hereditary conditions are known to decrease mitochondrial volume and function within skeletal muscle. This reduces endurance performance, and is manifest both at high- and low-intensity levels of exertion. A programme of regular endurance exercise, undertaken over a number of weeks, produces significant adaptations within skeletal muscle such that noticeable improvements in oxidative capacity are evident, and the related decline in endurance performance can be attenuated. Notwithstanding the important implications that this has for the highly trained endurance athlete, an improvement in mitochondrial volume and function through regular physical activity also endows the previously sedentary and/or aging population with an improved quality of life, and a greater functional independence. An understanding of the molecular and cellular mechanisms that govern the increases in mitochondrial volume with repeated bouts of exercise can provide insights into possible therapeutic interventions to care for those with mitochondrially-based diseases, and those unable to withstand regular physical activity. This review focuses on the recent developments in the molecular aspects of mitochondrial biogenesis in chronically exercising muscle. Specifically, we discuss the initial signalling events triggered by muscle contraction, the activation of transcription factors involved in both nuclear and mitochondrial DNA transcription, as well as the post-translational import mechanisms required for mitochondrial biogenesis. We consider the importance and relevance of chronic physical activity in the induction of mitochondrial biogenesis, with particular emphasis on how an endurance training programme could positively affect the age-related decline in mitochondrial content and delay the progression of age- and physical inactivity-related diseases.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a585bcee55c8a8dbffea79edbf7c889aTest
https://doi.org/10.2165/00007256-200333110-00001Test -
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المؤلفون: Paul A. Borsa, Linda M.-D. Nguyen, Kelly A. Larkin-Kaiser, Angelina G. Malamo, Peter J. Adhihetty
المصدر: Mitochondrion. 14(1)
مصطلحات موضوعية: chemistry.chemical_classification, Reactive oxygen species, Muscle Cells, biology, SIRT3, Infrared Rays, Cytochrome c, AMPK, Cell Biology, Mitochondrial Turnover, TFAM, medicine.disease_cause, Cell biology, Mitochondria, Mice, Mitochondrial biogenesis, chemistry, biology.protein, medicine, Molecular Medicine, Myocyte, Animals, Molecular Biology, Oxidative stress, Signal Transduction
الوصف: Near-infrared (NIR) light is a complementary therapy used to treat musculoskeletal injuries but the underlying mechanisms are unclear. Acute NIR light treatment (~800-950 nm; 22.8 J/cm(2)) induced a dose-dependent increase in mitochondrial signaling (AMPK, p38 MAPK) in differentiated muscle cells. Repeated NIR light exposure (4 days) appeared to elevate oxidative stress and increase the upstream mitochondrial regulatory proteins AMPK (3.1-fold), p38 (2.8-fold), PGC-1α (19.7%), Sirt1 (26.8%), and reduced RIP140 (23.2%), but downstream mitochondrial regulation/content (Tfam, NRF-1, Sirt3, cytochrome c, ETC subunits) was unaltered. Our data indicates that NIR light alters mitochondrial biogenesis signaling and may represent a mechanistic link to the clinical benefits.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c220f7758434e4085a05477aac4dabe3Test
https://pubmed.ncbi.nlm.nih.gov/24246911Test -
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المؤلفون: Scott K, Powers, Erin E, Talbert, Peter J, Adhihetty
المصدر: The Journal of physiology. 589(Pt 9)
مصطلحات موضوعية: NF-kappa B, Symposium Section Reviews: Reactive Oxygen and Nitrogen Species in Skeletal Muscle, Adaptation, Physiological, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Reactive Nitrogen Species, Oxidative Stress, Physical Endurance, Animals, Humans, Muscle, Skeletal, Reactive Oxygen Species, Oxidation-Reduction, Heat-Shock Proteins, Muscle Contraction, Signal Transduction, Transcription Factors
الوصف: It is well established that contracting skeletal muscles produce free radicals. Given that radicals are known to play a prominent role in the pathogenesis of several diseases, the 1980s-90s dogma was that contraction-induced radical production was detrimental to muscle because of oxidative damage to macromolecules within the fibre. In contrast to this early outlook, it is now clear that both reactive oxygen species (ROS) and reactive nitrogen species (RNS) play important roles in cell signalling pathways involved in muscle adaptation to exercise and the remodelling that occurs in skeletal muscle during periods of prolonged inactivity. This review will highlight two important redox sensitive signalling pathways that contribute to ROS and RNS-induced skeletal muscle adaptation to endurance exercise. We begin with a historical overview of radical production in skeletal muscles followed by a discussion of the intracellular sites for ROS and RNS production in muscle fibres. We will then provide a synopsis of the redox-sensitive NF-B and PGC-1α signalling pathways that contribute to skeletal muscle adaptation in response to exercise training. We will conclude with a discussion of unanswered questions in redox signalling in skeletal muscle in the hope of promoting additional research interest in this field.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=pmid________::88db89119182637df9f91c18cc697904Test
https://pubmed.ncbi.nlm.nih.gov/21224240Test -
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المؤلفون: Marco Colavecchia, David A. Hood, Isabella Irrcher, Sabena T Lowe, Anna-Maria Joseph, Joseph W. Gordon, Arne A. Rungi, Peter J. Adhihetty
المصدر: Medicine and science in sports and exercise. 35(1)
مصطلحات موضوعية: Transcriptional Activation, Protein Folding, Cell Respiration, Physical Therapy, Sports Therapy and Rehabilitation, Mitochondrial Membrane Transport Proteins, Translocation, Genetic, Mitochondrial Proteins, Mitochondrial membrane transport protein, Mitochondrial Precursor Protein Import Complex Proteins, Humans, Orthopedics and Sports Medicine, HSP70 Heat-Shock Proteins, Protein Precursors, Exercise, HSPA9, biology, Chaperonin 60, Mitochondrial carrier, Cell biology, Mitochondria, Muscle, mitochondrial fusion, Mitochondrial biogenesis, Translocase of the inner membrane, biology.protein, DNAJA3, ATP–ADP translocase, Carrier Proteins, Energy Metabolism, Molecular Chaperones, Muscle Contraction, Signal Transduction
الوصف: The importance of the mitochondrial protein import pathway, discussed relative to other steps involved in the overall biogenesis of the organelle, are reviewed.Mitochondrial biogenesis is a product of complex interactions between the nuclear and mitochondrial genomes. Signaling pathways, such as those activated by exercise, initiate the activation of transcription factors that increase the production of mRNA from nuclear and mitochondrial DNA. Nuclear gene products are translated in the cytosol as precursor proteins with inherent targeting signals. These precursor proteins interact with molecular chaperones that direct them to the import machinery of the outer membrane (Tom complex). The precursor is unfolded and transferred through the outer membrane, across the intermembrane space to the mitochondrial inner membrane translocases (Tim complex). Intramitochondrial components (mtHSP70) pull the precursor into the matrix, cleave off the targeting sequence (mitochondrial processing peptidase), and refold the protein (HSP60, cpn10) into its mature conformation. Physiological stressors such as contractile activity and thyroid hormone accelerate protein import into the mitochondria, coincident with an increase in the expression of some components of the import machinery. This is important for the overall expansion of the mitochondrial reticulum. Conversely, impairments in the import process can be a cause of mitochondrial dysfunction and disease.Efforts to further characterize the components of the import machinery, to define the role of specific machinery components on the import rate, and to examine protein import function in a variety of mitochondrial diseases are warranted.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8f019b09597ddf97c0553ad64f7dcbe8Test
https://pubmed.ncbi.nlm.nih.gov/12544641Test -
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المصدر: Experimental physiology. 88(1)
مصطلحات موضوعية: Aging, Biology, DNA, Mitochondrial, Endurance training, medicine, Animals, Humans, Exercise physiology, Muscle, Skeletal, Transcription factor, Exercise, chemistry.chemical_classification, Reactive oxygen species, Organelle Biogenesis, Skeletal muscle, General Medicine, Adaptation, Physiological, Cell biology, Nuclear DNA, Mitochondria, medicine.anatomical_structure, Biochemistry, chemistry, Mitochondrial biogenesis, Gene Expression Regulation, Physical Endurance, Organelle biogenesis, Muscle Contraction, Signal Transduction
الوصف: Regularly performed exercise in the form of endurance training produces a well-established adaptation in skeletal muscle termed mitochondrial biogenesis. The physiological benefit of this is an enhanced performance of muscle when subject to endurance exercise. This is not only of great advantage for athletic endeavours, but it also clearly improves the quality of life of previously sedentary individuals and those involved in injury rehabilitation. Here we review the molecular basis for mitochondrial biogenesis in muscle, from the initial signals arising in contracting muscle, to the transcription factors involved in mitochondrial and nuclear DNA transcription, as well as the post-translational import mechanisms required for the synthesis of the organelle. We discuss specific protein components associated with reactive oxygen species production, and suggest some questions which remain unanswered with respect to the role of exercise-induced mitochondrial biogenesis in ageing, apoptosis and disease.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::07bf38f4e238927a14775ee4d2e84be0Test
https://pubmed.ncbi.nlm.nih.gov/12525859Test -
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المؤلفون: Andy J Primeau, Peter J. Adhihetty, David A. Hood
المصدر: Canadian journal of applied physiology = Revue canadienne de physiologie appliquee. 27(4)
مصطلحات موضوعية: Programmed cell death, Physiology, Muscle Fibers, Skeletal, Apoptosis, Myocardial Reperfusion Injury, Mitochondrion, Muscular Dystrophies, medicine, In Situ Nick-End Labeling, Myocyte, Animals, Humans, Orthopedics and Sports Medicine, Myocytes, Cardiac, Muscle, Skeletal, Exercise, Caspase, Denervation, biology, business.industry, Cardiac muscle, Skeletal muscle, Mitochondria, Muscle, Oxidative Stress, medicine.anatomical_structure, Caspases, Hypertension, Ischemic Preconditioning, Myocardial, biology.protein, business, Reactive Oxygen Species, Neuroscience, Signal Transduction, Transcription Factors
الوصف: Apoptosis, or programmed cell death, is now recognized to be an important cellular event during normal development and in the progression of specific diseases. Apoptosis can be triggered by stimuli initiating outside of the cell, or within the mitochondria, leading to the activation of caspases and subsequent cell death. Although apoptosis has been widely studied in a variety of tissues over the last 5 years, skeletal muscle and heart have been relatively ignored in this regard. Research on apoptosis in cardiac muscle has recently taken on a higher profile as the recognition emerges that it may be an important contributor to specific cardiac pathologies, particularly in response to ischemia-reperfusion in which reactive oxygen species are formed. In skeletal muscle, very few studies have been done under specific physiological (e.g., exercise) and pathophysiological (e.g., dystrophies, denervation, myopathies) conditions. Skeletal muscle is unique in that it is mutli-nucleated, and evidence suggests that it can undergo individual myonuclear apoptosis as well as complete cell death. This review discusses the basic cellular mechanisms of apoptosis, as well as the current evidence of this process in cardiac and skeletal muscle. The need for more work in this area is highlighted, particularly in exercise and training. Key words: transcription factors, reactive oxygen species, mitochondria, caspase, mitochondrial permeability transition
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e219b6397aebfb69ab43e5648f0e2f82Test
https://pubmed.ncbi.nlm.nih.gov/12442352Test -
9
المؤلفون: Isabella Irrcher, T S. Sheehan, A-M Joseph, David A. Hood, Peter J. Adhihetty
المصدر: Medicine & Science in Sports & Exercise. 35:S123
مصطلحات موضوعية: Mitochondrial biogenesis, Chemistry, SOCS5, Physical Therapy, Sports Therapy and Rehabilitation, Orthopedics and Sports Medicine, SOCS6, Signal transduction, Protein expression, Cell biology
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::d764d38b7282edf68f2ab65d152ebeb7Test
https://doi.org/10.1097/00005768-200305001-00672Test
