Inflammation: Roles in Skeletal Muscle Atrophy

Antioxidants, Journal Year: 2022, Volume and Issue: 11(9), P. 1686 - 1686

Published: Aug. 29, 2022

Various diseases can cause skeletal muscle atrophy, usually accompanied by inflammation, mitochondrial dysfunction, apoptosis, decreased protein synthesis, and enhanced proteolysis. The underlying mechanism of inflammation in atrophy is extremely complex has not been fully elucidated, thus hindering the development effective therapeutic drugs preventive measures for atrophy. In this review, we elaborate on degradation pathways, including ubiquitin-proteasome system (UPS), autophagy-lysosome pathway (ALP), calpain caspase insulin growth factor 1/Akt synthesis pathway, myostatin, satellite cells, process Under an inflammatory environment, various pro-inflammatory cytokines directly act nuclear factor-κB, p38MAPK, JAK/STAT pathways through corresponding receptors, then are involved Inflammation also indirectly trigger changing metabolic state other tissues or cells. This paper explores changes hypothalamic-pituitary-adrenal axis fat metabolism under conditions as well their effects muscle. Moreover, reviews signaling related to conditions, such cachexia, sepsis, type 2 diabetes mellitus, obesity, chronic obstructive pulmonary disease, kidney nerve injury. Finally, summarizes anti-amyotrophic targets recent years. Overall, a key causing anti-inflammation might be strategy treatment factors downstream considered promising prevention

Language: Английский

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Physiology of sedentary behavior

Physiological Reviews, Journal Year: 2023, Volume and Issue: 103(4), P. 2561 - 2622

Published: June 16, 2023

Sedentary behaviors (SB) are characterized by low energy expenditure while in a sitting or reclining posture. Evidence relevant to understanding the physiology of SB can be derived from studies employing several experimental models: bed rest, immobilization, reduced step count, and reducing/interrupting prolonged SB. We examine physiological evidence relating body weight balance, intermediary metabolism, cardiovascular respiratory systems, musculoskeletal system, central nervous immunity inflammatory responses. Excessive lead insulin resistance, vascular dysfunction, shift substrate use toward carbohydrate oxidation, muscle fiber oxidative glycolytic type, cardiorespiratory fitness, loss mass strength bone mass, increased total fat visceral depot, blood lipid concentrations, inflammation. Despite marked differences across individual studies, longer term interventions aimed at have resulted small, albeit marginally clinically meaningful, benefits on weight, waist circumference, percent fat, fasting glucose, insulin, HbA1c HDL systolic pressure, function adults older adults. There is more limited for other health-related outcomes systems children adolescents. Future research should focus investigation molecular cellular mechanisms underpinning adaptations increasing necessary changes physical activity impact overall health diverse population groups.

Language: Английский

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Oxidative stress: Roles in skeletal muscle atrophy

Biochemical Pharmacology, Journal Year: 2023, Volume and Issue: 214, P. 115664 - 115664

Published: June 16, 2023

Language: Английский

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Skeletal muscle oxidative stress and inflammation in aging: Focus on antioxidant and anti-inflammatory therapy

Frontiers in Cell and Developmental Biology, Journal Year: 2022, Volume and Issue: 10

Published: Aug. 30, 2022

With aging, the progressive loss of skeletal muscle will have negative effect on multiple physiological parameters, such as exercise, respiration, thermoregulation, and metabolic homeostasis. Accumulating evidence reveals that oxidative stress inflammation are main pathological characteristics during aging. Here, we focus aging-related sarcopenia, summarize relationship between aging elaborate aging-mediated damage in its critical role occurrence development sarcopenia. In addition, discuss production excessive reactive oxygen species muscle, which reduces ability satellite cells to participate regeneration, analyze potential molecular mechanism ROS-mediated mitochondrial dysfunction muscle. Furthermore, also paid extensive attention possibility regulatory pathways mediate inflammation. Finally, response abnormal activity several antioxidant anti-inflammatory strategies for treatment may provide beneficial help improving sarcopenia

Language: Английский

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Mitochondrial dysfunction and skeletal muscle atrophy: Causes, mechanisms, and treatment strategies

Mitochondrion, Journal Year: 2023, Volume and Issue: 72, P. 33 - 58

Published: July 13, 2023

Language: Английский

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Fiber-Type Shifting in Sarcopenia of Old Age: Proteomic Profiling of the Contractile Apparatus of Skeletal Muscles

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(3), P. 2415 - 2415

Published: Jan. 26, 2023

The progressive loss of skeletal muscle mass and concomitant reduction in contractile strength plays a central role frailty syndrome. Age-related neuronal impairments are closely associated with sarcopenia the elderly, which is characterized by severe muscular atrophy that can considerably lessen overall quality life at old age. Mass-spectrometry-based proteomic surveys senescent human muscles, as well animal models sarcopenia, have decisively improved our understanding molecular cellular consequences fiber-type shifting during aging. This review outlines spectrometric identification proteome-wide changes atrophying focus on proteins potential markers distribution patterns. observed trend fast-to-slow transitions individual muscles aging process most likely linked to preferential susceptibility fast-twitching fibers atrophy. Studies models, including mostly aged rodent confirmed shifting. analysis fast versus slow isoforms key proteins, such myosin heavy chains, light actins, troponins tropomyosins, suggests them suitable bioanalytical tools

Language: Английский

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Diet, exercise, and pharmacotherapy for sarcopenia in people with diabetes

Metabolism, Journal Year: 2023, Volume and Issue: 144, P. 155585 - 155585

Published: May 6, 2023

Language: Английский

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Anti-atrophic Role of Ononis natrix subsp. hispanica Extract in Skeletal Muscle Atrophy: Pathway-targeted Insights and Experimental Validation

Food Bioscience, Journal Year: 2025, Volume and Issue: unknown, P. 106000 - 106000

Published: Jan. 1, 2025

Language: Английский

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Forkhead Box O Signaling Pathway in Skeletal Muscle Atrophy

American Journal Of Pathology, Journal Year: 2022, Volume and Issue: 192(12), P. 1648 - 1657

Published: Sept. 27, 2022

Skeletal muscle atrophy is the consequence of protein degradation exceeding synthesis because disease, aging, and physical inactivity. Patients with skeletal have decreased mass fiber cross-sectional area, experience reduced survival quality motor function. The forkhead box O (FOXO) signaling pathway plays an important role in pathogenesis by regulating E3 ubiquitin ligases some autophagy factors. However, mechanism FOXO leading to still unclear. development treatment strategies for has been a thorny clinical problem. FOXO-targeted therapy treat promising approach, increasing number relevant studies reported. This article reviews therapeutic targets mediating atrophy, provides ideas this condition. most abundant tissue human body, accounting 40% 50% total healthy individual.1Sartori R. Romanello V. Sandri M. Mechanisms hypertrophy: implications health disease.Nat Commun. 2021; 12: 330Crossref PubMed Scopus (138) Google Scholar It not only controls movement, but also participates multiple life activities, including breathing, eating, energy consumption, nutrient metabolism.1Sartori loss volume inactivity, aging known as characterized area content.1Sartori Scholar, 2Kandarian S.C. Jackman R.W. Intracellular during atrophy.Muscle Nerve. 2006; 33: 155-165Crossref (282) 3Miller S.G. Hafen P.S. Brault J.J. Increased adenine nucleotide atrophy.Int J Mol Sci. 2020; 21: 88Crossref (18) may cause reduction function life.3Miller There are many diseases that can such diabetes cachexia, which significantly affect prognosis patients increase mortality.4Reed S.A. Sandesara P.B. Senf S.M. Judge A.R. Inhibition FoxO transcriptional activity prevents cachexia induces hypertrophy.FASEB J. 2011; 26: 987-1000Crossref (0) Scholar,5O'Neill B.T. Bhardwaj G. Penniman C.M. Krumpoch M.T. Suarez Beltran P.A. Klaus K. Poro Li Pan H. Dreyfuss J.M. Nair K.S. Kahn C.R. transcription factors critical regulators diabetes-related atrophy.Diabetes. 2019; 68: 556-570Crossref (68) itself threatening, its complications (such osteoporosis, blood clots, pressure sores) lead morbidity mortality.6Cao R.Y. Dai Q. Yang Muscle atrophy: present future.Adv Exp Med Biol. 2018; 1088: 605-624Crossref (12) common practice, largely limited traditional methods, exercise nutritional supplementation, no effective treatment.7Yin L. N. Jia W. Wang Liang X. Du from mechanisms treatments.Pharmacol Res. 172: 105807Crossref (13) Therefore, it imperative find new or drugs atrophy. insulin-like growth factor-1/phosphatidylinositol-3-hydroxykinase/V-akt murine thymoma viral oncogene homolog (IGF-1/PI3K/AKT) pathway, be activated cellular stimulation toxic injury, regulates essential functions transcription, translation, proliferation, growth, survival. Besides aforementioned functions, IGF-1/PI3K/AKT gain mass.8Léger B. Cartoni Praz Lamon S. Dériaz O. Crettenand A. Gobelet C. Rohmer P. Konzelmann Luthi F. Russell A.P. Akt signalling through GSK-3beta, mTOR Foxo1 involved hypertrophy atrophy.J Physiol. 576: 923-933Crossref Activation AKT key processes phosphorylating substrates apoptosis, synthesis, metabolism, cell cycle.9Timmer L.T. Hoogaars W.M.H. Jaspers R.T. IGF-1 atrophy.Adv 109-137Crossref (25) Downstream include glycogen synthase kinase-3β, mammalian target rapamycin (mTOR), (FOXO), all regulatory proteins atrophy.8Léger 9Timmer 10Stitt T.N. Drujan D. Clarke B.A. Panaro Timofeyva Y. Kline W.O. Gonzalez Yancopoulos G.D. Glass D.J. IGF-1/PI3K/Akt expression atrophy-induced inhibiting factors.Mol Cell. 2004; 14: 395-403Abstract Full Text PDF (1463) 11Yoshida T. Delafontaine IGF-1-mediated regulation atrophy.Cells. 9: 1970Crossref (92) FOXOs evolutionarily conserved metabolic stress responses.12Monsalve Olmos complex biology FOXO.Curr Drug Targets. 1322-1350Crossref (94) Four types identified namely, FOXO1, FOXO3, FOXO4, FOXO6.13Calissi Lam E.W. Link Therapeutic targeting factors.Nat Rev Discovery. 20: 21-38Crossref Of these, FOXO1 FOXO3 primarily atrophy.14Kang Lee Kim E. Sohn U.D. I. Forkhead O3 e3 MuRF-1 atrogin-1 Cushing's syndrome.Am Physiol Endoc 2017; 312: E495-E507Crossref Scholar,15Oyabu Takigawa Mizutani Hatazawa Fujita Ohira Sugimoto Suzuki Tsuchiya Suganami Ogawa Ishihara Miura Kamei cooperates C/EBPδ ATF4 regulate program fasting.FASEB 2022; 36: e22152Crossref (3) By summarizing possible aims provide future treatment. primary secondary atrophy.7Yin Primary includes muscular dystrophy, congenital myopathy, mitochondrial myopathy,7Yin whereas pathologic conditions neuromuscular diseases, cancer, chronic inflammatory acute illness.7Yin Scholar,16Powers Lynch G.S. Murphy K.T. Reid M.B. Zijdewind Disease-induced fatigue.Med Sci Sports Exerc. 2016; 48: 2307-2319Crossref (85) Regardless pathogenesis, stability result balance between anabolism catabolism, covering both direct indirect factors.17Wang Pessin J.E. fiber-type specificity atrophy.Curr Opin Clin Nutr. 2013; 16: 243-250Crossref Scholar,18Wilburn Ismaeel Machek Fletcher Koutakis Shared distinct narrative review.Ageing Res Rev. 71: 101463Crossref driven hormone, insulin, IGF-1, testosterone, catabolism regulated endocrine, inflammatory, oxidative factors.19Malavaki C.J. Sakkas G.K. Mitrou G.I. Kalyva Stefanidis Myburgh K.H. Karatzaferi disease-induced mask disuse Cell 405-421Crossref (32) proteolytic systems [namely, proteasome system (UPS), lysosome system, cysteine aspartic proteases, calpain system].1Sartori Scholar,7Yin related UPS system. Different genes autophagy. composed activase, ubiquitin-binding enzyme, ligase (E3), ubiquitin, 26S proteasome.20Park Cho Song E.J. Ubiquitin–proteasome (UPS) anticancer treatment.Arch Pharm 43: 1144-1161Crossref (2) Among ring finger 1 (MuRF-1) F-box (MAFbx)/Atrogin-1, ubiquitinates desmin downstream pathway. significant factor myofibril degradation. Atrogin-1 Ubiquitin forms compounds activase enzyme sequence, transfers processing, where finally degraded proteasome, peptide release recycling.7Yin Bnip3, Gabarap, LC3, Atg12.21Rocchi He Regulation exercise-induced muscle.Curr Pathobiol Rep. 5: 177-186Crossref homeostasis.22Sartorelli Fulco Molecular determinants hypertrophy.Science's STKE. 2004: re11Crossref two main branches AKT-activated AKT-blocked kinase-3β (GSK-3β), influence synthesis.23Rodriguez Vernus Chelh Cassar-Malek Gabillard J.C. Hadj Sassi Picard Bonnieu Myostatin pathways.Cell Life 2014; 4361-4371Crossref (218) Scholar,24Sandri Signaling hypertrophy.Physiology. 2008; 23: 160-170Crossref (606) GSK-3β block eukaryotic initiation 2B, synthesis. activates translation factor, resulting increased synthesis.22Sartorelli kinase interacts several form complexes: rapamycin-sensitive (mTORC1) containing Raptor, rapamycin-insensitive mTORC2 Rictor.1Sartori mTORC1 mainly Phosphorylation mediated Raptor-interacting inhibit 4E binding (4EBP1). mTORC1-mediated inhibition 4EBP1 further leads activation 4E, thereby synthesis.3Miller Scholar,22Sartorelli phosphorylation p70 ribosomal S6 kinase.3Miller detailed shown Figure 1. one major pathway.25Zhang Tang Hadden T.J. Rishi A.K. Akt, apoptosis.Biochim Biophys Acta. 1813: 1978-1986Crossref (713) first gene region was discovered 1989 Weigel et al26Weigel Jürgens Küttner Seifert Jäckle homeotic fork head encodes nuclear expressed terminal regions Drosophila embryo.Cell. 1989; 57: 645-658Abstract (608) while studying Drosophila. responses, responsible associated autophagy, stress, atrophy.12Monsalve Scholar,27Bhardwaj Jena B.P. Foster Junck T.L. Hinton A.O. Souvenir Fuqua J.D. Morales P.E. Bravo-Sagua Sivitz W.I. Lira V.A. Abel E.D. O'Neill Insulin receptors I-dependent bioenergetics supercomplexes via FoxOs muscle.J Invest. 131: e146415Crossref (4) identified, FOXO6, belong large family share highly 100 amino acid DNA domain called domain.13Calissi extensively muscle14Kang Scholar; FOXO4 cardiac muscle; FOXO6 brain.12Monsalve variety external stimuli, other factors, neurotrophic cytokines, stimuli.28Calnan D.R. Brunet code.Oncogene. 27: 2276-2288Crossref (901) these stimuli achieved alterations posttranslational modifications FOXOs, phosphorylation, acetylation, ubiquitination modifications.29Link Introduction biology.Methods 1890: 1-9Crossref (70) predominant modification kinases, AKT, AMP-activated kinase, c-Jun N-terminal arginine methyltransferase, serum- glucocorticoid-inducible extracellular signal-regulated p38, cyclin-dependent 2, casein 1, STE20-like each recognizing specific sequence FOXO.13Calissi particular input signal presence factors.29Link their translocation cytoplasm subsequent inactivation.30Cheng Z. FoxO–autophagy axis disease.Trends Endocrinol Metab. 30: 658-671Abstract Scholar,31Farhan Gaur U. Little P.J. Xu Zheng pathways cancer.Int Biol 13: 815-827Crossref (212) on induction kinases (eg, kinase/AMPK), translocated nucleus, they perform functions.30Cheng dephosphorylated up-regulate various p21 p27, cycle; FasL, Bim, Atg, apoptosis autophagy; G6P, involves gluconeogenesis; Pomc AgRP, food intake; Atrogin-1, causes atrophy).28Calnan Because range biological processes, studied. According Alvarez-Garcia al,32Alvarez-Garcia Matsuzaki Olmer Miyata Mokuda Sakai Masuda Asahara Lotz M.K. required intervertebral disk homeostasis deficiency promotes degeneration.Aging 17: e12800Crossref delays disc degeneration aging. Xin al33Xin Ma Jiang Fan Di Hu She impaired heart: diseases.Biochim Acta Basis Dis. 1863: 486-498Crossref (36) indicate play generation diseases. Rajendran al34Rajendran N.K. Dhilip Kumar S.S. Houreld N.N. Abrahamse Understanding perspectives delayed wound healing.J Commun Signaling. 151-162Crossref suggest molecules influencing physiological healing. Reed al4Reed showed cachexia-induced neurodegenerative diseases,35Hu Han Yu Shen Roles o (FoxO) diseases: panoramic view.Prog Neurobiol. 181: 101645Crossref Alzheimer disease,36Zhou Bai Zhong Zhang Kang Zhao Downregulation PIK3CB Alzheimer's disease axon guidance, pathway.Oxid Longev. 2022: 1-15Google depression,37Rana Behl Sehgal Mehta Singh Sharma Bungau Elucidating depression.Neurochem 46: 2761-2775Crossref (5) type 2 diabetes,38Horiguchi Turudome Ushijima transplantation resistance II mellitus adipose-derived stem cells due G6PC IGF1 pathway.Int 22: 6595Crossref (1) cancer,39Chen Y.H. C.L. Chen W.J. Liu Wu H.T. Diverse roles members gastric cancer.World Gastrointest Oncol. 1367-1382Crossref 40Ghaffarnia Nasrollahzadeh Bashash Mousavi Ghaffari S.H. c-Myc using 10058-f4 anti-tumor effects ovarian cancer genes.Eur Pharmacol. 908: 174345Crossref 41Wang Luo Akinyemiju Hwang Yue Wei Association genetic variants FBXO32 breast risk.Mol Carcinog. 60: 661-670Crossref more. As mentioned above, underlying link described next. In 2004, al42Kamei Kai Mizukami Taniguchi Mochida Hata Matsuda Aburatani Nishino Ezaki (FKHR) transgenic mice less mass, down-regulated I (slow twitch/red muscle) genes, glycemic control.J Chem. 279: 41114-41123Abstract (430) demonstrated negatively establishing overexpression mouse models. remains al43Sandri Gilbert Skurk Calabria Walsh Schiaffino Lecker Goldberg A.L. Foxo induce atrophy-related atrophy.Cell. 117: 399-412Abstract (2174) They concluded that, normally growing muscle, upstream suppresses FOXO-mediated atrophy.43Sandri action attributed transferred inactivated.16Powers al14Kang proposed glucocorticoid receptor act rat model Cushing syndrome. authors pointed out Atrogin-1.14Kang A group novel FOXO, MUSA1, SMART, FBXO31, Itch, were recent closely atrophy.44Brocca Toniolo Reggiani Bottinelli Pellegrino M.A. FoxO-dependent atrogenes vary among catabolic induced hindlimb suspension.J 595: 1143-1158Crossref (48) 45Milan Pescatore Armani Paik Frasson Seydel Abraham Blaauw DePinho R.A. ubiquitin–proteasome network atrophy.Nat 2015; 6: 6670Crossref 46Sartori Schirwis Bortolanza Enzo Stantzou Mouisel Ferry Stricker Dupont Piccolo Amthor BMP mass.Nat Genet. 45: 1309-1318Crossref (284) addition genes.47Ji L.L. Yeo caused discord intracellular signaling.Antioxid Redox Sign. 727-744Crossref (6) 48Mammucari Milan Masiero Rudolf Del Burden S.J. Lisi FoxO3 vivo.Cell 2007; 458-471Abstract (1424) 49Zhao Schild Cao c

Language: Английский

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Diabetic Muscular Atrophy: Molecular Mechanisms and Promising Therapies

Frontiers in Endocrinology, Journal Year: 2022, Volume and Issue: 13

Published: June 30, 2022

Diabetes mellitus (DM) is a typical chronic disease that can be divided into 2 types, dependent on insulin deficiency or resistance. Incidences of diabetic complications gradually increase as the progresses. Studies in diabetes have mostly focused kidney and cardiovascular diseases, well neuropathy. However, DM also cause skeletal muscle atrophy. Diabetic muscular atrophy an unrecognized complication lead to quadriplegia severe cases, seriously impacting patients’ quality life. In this review, we first identify main molecular mechanisms from aspects protein degradation synthesis signaling pathways. Then, discuss regulatory atrophy, outline potential drugs treatments terms resistance, deficiency, inflammation, oxidative stress, glucocorticoids, other factors. It worth noting inflammation stress are closely related resistance Regulating may represent another very important way treat addition controlling signaling. Understanding mechanism could help reveal new treatment strategies.

Language: Английский

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