Aging, Skeletal Muscle, and Epigenetics.
Journal
Plastic and reconstructive surgery
ISSN: 1529-4242
Titre abrégé: Plast Reconstr Surg
Pays: United States
ID NLM: 1306050
Informations de publication
Date de publication:
01 10 2022
01 10 2022
Historique:
entrez:
28
9
2022
pubmed:
29
9
2022
medline:
1
10
2022
Statut:
ppublish
Résumé
We are living in an aging society. In 2019, 1 billion individuals were already aged over 60. The number of people in this demographic is predicted to reach 1.4 billion by 2030 and 2.1 billion by 2050 (WHO). In the USA, individuals over 65 represent the fastest growing segment of the population (US census bureau). Similar trends are seen in the UK, with 16.2 million people already aged over 60, equivalent to 24% of the total population (Age UK; https://www.ageuk.org.uk/globalassets/age-uk/documents/reports-and-publications/later_life_uk_factsheet.pdf). Indeed, in the UK, people over the age of 60 outnumbered those under the age of 18, for the first time in 2008. This statistic still prevails today. Because of medical and biopharmaceutical progress, lifespan is increasing rapidly, but healthspan is failing to keep up. If we are to increase healthy living, then we need to begin to understand the mechanisms of how we age across the life course, so that relevant interventions may be developed to facilitate "life in our years," not simply "years in our life." It is reported that only 25% of aging is genetically predetermined. This fits with observations of some families aging very quickly and poorly and others aging slowly and well. If this is indeed the case and the rate of aging is not fixed, then this knowledge provides a significant opportunity to manipulate the impact of environmental influencers of age. With that in mind, it begs the question of what are the mechanisms of aging and is there potential to manipulate this process on an individual-by-individual basis? The focus of this article will be on the process of muscle wasting with aging (sarcopenia) and the potential of exercise and its underlying mechanisms to reverse or delay sarcopenia. There will be a focus on epigenetics in muscle wasting and the capability of exercise to change our skeletal muscle epigenetic profile for the good. The article ends with considerations relating to facial aging, Botox treatment, and gene editing as a tool for plastic surgeons in the future.
Identifiants
pubmed: 36170433
doi: 10.1097/PRS.0000000000009670
pii: 00006534-202210002-00006
doi:
Substances chimiques
Biological Products
0
Botulinum Toxins, Type A
EC 3.4.24.69
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
27S-33SInformations de copyright
Copyright © 2022 by the American Society of Plastic Surgeons.
Références
Garatachea N, Pareja-Galeano H, Sanchis-Gomar F, et al. Exercise attenuates the major hallmarks of aging. Rejuvenation Res. 2015;18:57–89.
López-Otín C, Blasco MA, Partridge L, et al. The hallmarks of aging. Cell. 2013;153:1194–1217.
McKendry J, Currier BS, Lim C, et al. Nutritional supplements to support resistance exercise in countering the sarcopenia of aging. Nutrients. 2020;12:E2057.
Phillips SM, Parise G, Roy BD, et al. Resistance-training-induced adaptations in skeletal muscle protein turnover in the fed state. Can J Physiol Pharmacol. 2002;80:1045–1053.
Jacobs BL, You JS, Frey JW, et al. Eccentric contractions increase the phosphorylation of tuberous sclerosis complex-2 (TSC2) and alter the targeting of TSC2 and the mechanistic target of rapamycin to the lysosome. J Physiol. 2013;591:4611–4620.
Wolfson RL, Chantranupong L, Saxton RA, et al. Sestrin2 is a leucine sensor for the mTORC1 pathway. Science. 2016;351:43–48.
Cermak NM, Res PT, de Groot LC, et al. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: A meta-analysis. Am J Clin Nutr. 2012;96:1454–1464.
Drummond MJ, Dreyer HC, Pennings B, et al. Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging. J Appl Physiol (1985). 2008;104:1452–1461.
Yang Y, Breen L, Burd NA, et al. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men. Br J Nutr. 2012;108:1780–1788.
Bentzinger CF, Lin S, Romanino K, et al. Differential response of skeletal muscles to mTORC1 signaling during atrophy and hypertrophy. Skelet Muscle. 2013;3:6.
Castets P, Lin S, Rion N, et al. Sustained activation of mTORC1 in skeletal muscle inhibits constitutive and starvation-induced autophagy and causes a severe, late-onset myopathy. Cell Metab. 2013;17:731–744.
Joseph GA, Wang SX, Jacobs CE, et al. Partial inhibition of mTORC1 in Aged rats counteracts the decline in muscle mass and reverses molecular signaling associated with sarcopenia. Mol Cell Biol. 2019;39:e00141–e00119.
Vellai T, Takacs-Vellai K, Zhang Y, et al. Genetics: influence of TOR kinase on lifespan in C. elegans. Nature. 2003;426:620.
Harrison DE, Strong R, Sharp ZD, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. 2009;460:392–395.
Weichhart T. mTOR as Regulator of lifespan, aging, and cellular senescence: A mini-review. Gerontology. 2018;64:127–134.
Kalender A, Selvaraj A, Kim SY, et al. Metformin, independent of AMPK, inhibits mTORC1 in a rag GTPase-dependent manner. Cell Metab. 2010;11:390–401.
Glossmann HH, Lutz OMD. Metformin and aging: A review. Gerontology. 2019;65:581–590.
Kirwan R, McCullough D, Butler T, et al. Sarcopenia during COVID-19 lockdown restrictions: Long-term health effects of short-term muscle loss. Geroscience. 2020;42:1547–1578.
Sayer AA, Syddall H, Martin H, et al. The developmental origins of sarcopenia. J Nutr Health Aging. 2008;12:427–432.
Kim YK, Lee HS, Ryu JJ, et al. Sarcopenia increases the risk for mortality in patients who undergo amputation for diabetic foot. J Foot Ankle Res. 2018;11:32.
Jones PL, Veenstra GJ, Wade PA, et al. Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription. Nat Genet. 1998;19:187–191.
Bogdanović O, Veenstra GJ. DNA methylation and methyl-CpG binding proteins: developmental requirements and function. Chromosoma. 2009;118:549–565.
Zykovich A, Hubbard A, Flynn JM, et al. Genome-wide DNA methylation changes with age in disease-free human skeletal muscle. Aging Cell. 2014;13:360–366.
Voisin S, Harvey NR, Haupt LM, et al. An epigenetic clock for human skeletal muscle. J Cachexia Sarcopenia Muscle. 2020;11:887–898.
Voisin S, Jacques M, Landen S, et al. Meta-analysis of genome-wide DNA methylation and integrative omics of age in human skeletal muscle. J Cachexia Sarcopenia Muscle. 2021;12:1064–1078.
Turner DC, Gorski PP, Maasar MF, et al. DNA methylation across the genome in aged human skeletal muscle tissue and muscle-derived cells: The role of HOX genes and physical activity. Sci Rep. 2020;10:15360.
Sharples AP, Polydorou I, Hughes DC, et al. Skeletal muscle cells possess a “memory” of acute early life TNF-α exposure: Role of epigenetic adaptation. Biogerontology. 2016;17:603–617.
Sailani MR, Halling JF, Møller HD, et al. Lifelong physical activity is associated with promoter hypomethylation of genes involved in metabolism, myogenesis, contractile properties and oxidative stress resistance in aged human skeletal muscle. Sci Rep. 2019;9:3272.
Seaborne RA, Strauss J, Cocks M, et al. Human skeletal muscle possesses an epigenetic memory of hypertrophy. Sci Rep. 2018;8:1898.
Wen Y, Dungan CM, Mobley CB, et al. Nucleus type-specific DNA methylomics reveals epigenetic “memory” of prior adaptation in skeletal muscle. Function (Oxf). 2021;2:zqab038.
Sharples AP. Skeletal muscle possesses an epigenetic memory of exercise: Role of nucleus type-specific DNA methylation. Function (Oxf). 2021;2:zqab047.
Turner DC, Seaborne RA, Sharples AP. Comparative transcriptome and methylome analysis in human skeletal muscle anabolism, hypertrophy and epigenetic memory. Sci Rep. 2019;9:4251.
Blocquiaux S, Ramaekers M, Van Thienen R, et al. Recurrent training rejuvenates and enhances transcriptome and methylome responses in young and older human muscle. JCSM Rapid Communications. 2022;5:10–32.
Ruple BA, Godwin JS, Mesquita PHC, et al. Resistance training rejuvenates the mitochondrial methylome in aged human skeletal muscle. FASEB J. 2021;35:e21864.
Orioli D, Dellambra E. Epigenetic regulation of skin cells in natural aging and premature aging diseases. Cells. 2018;7:E268.
Swift A, Liew S, Weinkle S, et al. The facial aging process from the “inside out”. Aesthet Surg J. 2021;41:1107–1119.
Nassif AD, Boggio RF, Espicalsky S, et al. high precision use of botulinum toxin type A (BONT-A) in aesthetics based on muscle atrophy, is muscular architecture reprogramming a possibility? A systematic review of literature on muscle atrophy after BoNT-A injections. Toxins (Basel). 2022;14:81.
Borodic GE, Ferrante R. Effects of repeated botulinum toxin injections on orbicularis oculi muscle. J Clin Neuroophthalmol. 1992;12:121–127.
Schroeder AS, Ertl-Wagner B, Britsch S, et al. Muscle biopsy substantiates long-term MRI alterations one year after a single dose of botulinum toxin injected into the lateral gastrocnemius muscle of healthy volunteers. Mov Disord. 2009;24:1494–1503.
Roh DS, Li EB, Liao EC. CRISPR Craft: DNA editing the reconstructive ladder. Plast Reconstr Surg. 2018;142:1355–1364.
Baker DJ, Dawlaty MM, Wijshake T, et al. Increased expression of BubR1 protects against aneuploidy and cancer and extends healthy lifespan. Nat Cell Biol. 2013;15:96–102.
Callaway E. Telomerase reverses ageing process. Nature. November 28, 2010.
Köhler F, Bormann F, Raddatz G, et al. Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford progeria syndrome. Genome Med. 2020;12:46.
Hipp MS, Kasturi P, Hartl FU. The proteostasis network and its decline in ageing. Nat Rev Mol Cell Biol. 2019;20:421–435.
Johnson SC. Nutrient sensing, signaling and ageing: The role of IGF-1 and mTOR in ageing and age-related disease. Harris JR, Korolchuk VI, eds. In: Biochemistry and Cell Biology of Ageing: Part I Biomedical Science. Singapore: Springer Singapore; 2018:49–97.
Ferrucci L, Zampino M. A mitochondrial root to accelerated ageing and frailty. Nat Rev Endocrinol. 2020;16:133–134.
Wang MJ, Chen J, Chen F, et al. Rejuvenating strategies of tissue-specific stem cells for healthy aging. Aging Dis. 2019;10:871–882.
Fafián-Labora JA, O’Loghlen A. Classical and nonclassical intercellular communication in senescence and ageing. Trends Cell Biol. 2020;30:628–639.