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CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function
Open accessAbstract
MyoD , a master regulator of myogenesis, exhibits a circadian rhythm in its mRNA and protein levels, suggesting a possible role in the daily maintenance of muscle phenotype and function. We report that MyoD is a direct target of the circadian transcriptional activators CLOCK and BMAL1, which bind in a rhythmic manner to the core enhancer of the MyoD promoter. Skeletal muscle of Clock Δ19 and Bmal1 −/− mutant mice exhibited ∼30% reductions in normalized maximal force. A similar reduction in force was observed at the single-fiber level. Electron microscopy (EM) showed that the myofilament architecture was disrupted in skeletal muscle of Clock Δ19 , Bmal1 −/− , and MyoD −/− mice. The alteration in myofilament organization was associated with decreased expression of actin, myosins, titin, and several MyoD target genes. EM analysis also demonstrated that muscle from both Clock Δ19 and Bmal1 −/− mice had a 40% reduction in mitochondrial volume. The remaining mitochondria in these mutant mice displayed aberrant morphology and increased uncoupling of respiration. This mitochondrial pathology was not seen in muscle of MyoD −/− mice. We suggest that altered expression of both Pgc-1α and Pgc-1β in Clock Δ19 and Bmal1 −/− mice may underlie this pathology. Taken together, our results demonstrate that disruption of CLOCK or BMAL1 leads to structural and functional alterations at the cellular level in skeletal muscle. The identification of MyoD as a clock-controlled gene provides a mechanism by which the circadian clock may generate a muscle-specific circadian transcriptome in an adaptive role for the daily maintenance of adult skeletal muscle.
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“The functional significance of disrupting the molecular clock has been shown in genetic mouse models (i.e., Clock mutant mice and the Bmal1 KO mouse), which display reduced glucose tolerance, mitochondrial respiratory function, and skeletal muscle contractile function [20,21].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [21]
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“Considering the negative metabolic consequences, such as reduction in insulin sensitivity and mitochondrial function, attributed to both circadian misalignment and sleep loss [21,67] and the potential benefits of exercise in this context [17,68], further research is warranted.”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [21]
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Citations
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BackgroundThe Nuclear Receptor and Clock Repressor Rev-erbα Suppresses Myogenesis
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Zhu, P., Hamlish, N. X., Thakkar, A. V., Steffeck, A. W. T., Rendleman, E. J., Khan, N. H., Waldeck, N. J., DeVilbiss, A., Martin-Sandoval, M. S., Mathews, T. P., et al. (2022) · Genes & Development · doi:10.1101/gad.349066.121 · Cited by 46
“One reason for this could be premature activation of MRFs, and previous studies have shown conflicting results on the effect of Bmal1 loss on MRF expression (e.g., Myf5 , MyoD , and myogenin ) (Andrews et al. 2010; Chatterjee et al. 2013).”
Rivera-Reyes, A., Ye, S., Marino, G. E., Egolf, S., Ciotti, G. E., Chor, S., Liu, Y., Posimo, J. M., Park, P. M. C., Pak, K., et al. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-1142-4 · Cited by 43
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“Circadian control of β-cell mitochondrial metabolism has not been studied although there is evidence that the circadian clock regulates mitochondrial metabolism in heart [67] and skeletal muscle [68].”
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Diurnal Control of Blood Pressure Is Uncoupled From Sodium Excretion
Johnston, J. G., Speed, J. S., Becker, B., Kasztan, M., Soliman, R. H., Rhoads, M. K., Tao, B., Jin, C., Geurts, A. M., Hyndman, K. A., et al. (2020) · Hypertension · doi:10.1161/hypertensionaha.119.13908 · Cited by 39
“numerous pathophysiological phenotypes, such as skeletal muscle weakness and impaired glucose homeostasis.(19,20) Bmal1 mice generally lack circadian rhythms in a wide range of physiological variables including BP that is char-”
BackgroundDaily running enhances molecular and physiological circadian rhythms in skeletal muscle
Casanova-Vallve, N., Duglan, D., Vaughan, M. E., Pariollaud, M., Handzlik, M. K., Fan, W., Yu, R. T., Liddle, C., Downes, M., Delezie, J., et al. (2022) · Molecular Metabolism · doi:10.1016/j.molmet.2022.101504 · Cited by 42
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Self-citationCircadian regulation of muscle growth independent of locomotor activity
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“Murine whole-body knockout of the core clock gene Bmal1 results in severe defects in growth and muscle function (12, 13), but muscle-specific Bmal1 knockout failed to recapitulate these phenotypes (14, 15), suggesting they might be secondary to clock disruption in other tissues.”
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“Indeed, animal models have indicated a circadian variation in the mRNA expression of the myogenic regulatory factors MyoD, myogenin, MuRF1, Akt1, and ribosomal protein S6, and also in phosphorylated levels of Akt and ribosomal protein S6 in rodent skeletal muscle (Andrews et al. 2010; Shavlakadze et al. 2013).”
BackgroundDifferential roles for cryptochromes in the mammalian retinal clock
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Exercise as a Peripheral Circadian Clock Resynchronizer in Vascular and Skeletal Muscle Aging
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“Interestingly, Clock- and BMAL1 gene mutant mice exhibit approximately 30% reductions in maximum muscle strength and 40% in mitochondrial volume [12].”
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Synaptic BMAL1 phosphorylation controls circadian hippocampal plasticity
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“As seen in the volcano plot (Supplementary Figure 5A) and consistent with prior studies [4 e 6], many of the clock output genes, such as Dbp , Mylk4 , and Tcap were signi fi cantly down-regulated [39,40].”
ResultSelf-citationA Novel Link Between Circadian Clocks and Adipose Tissue Energy Metabolism
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“In skeletal muscle, CLOCK and BMAL1 are essential for the maintenance of normal mitochondrial biogenesis and respiratory function (13).”
BackgroundMuscle–bone interactions: movement in the field of mechano–humoral coupling of muscle and bone
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Self-citationCircadian rhythm of intracellular protein synthesis signaling in rat cardiac and skeletal muscles
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“The loss of these clock genes influences the function and growth of the liver, cardiac, and skeletal muscles of mice [3,6,7].”
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“The impaired cell structure and function of the skeletal muscle in the global Bmal1 KO mice was demonstrated [9].”
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“…or hormones regulation (i.e., cortisol, melatonin) (Selmaoui and Touitou 2003), which affect the molecular clock in skeletal muscle (Schroder and Esser 2013) influencing muscle contraction potentially by causing a reduction in maximal force production (Andrews et al. 2010; Chtourou et al. 2012).”
BackgroundTargeted Bmal1 restoration in muscle prolongs lifespan with systemic health effects in aging model
Gutierrez‐Monreal, M. A., Wolff, C. A., Rijos, E. E., Viggars, M. R., Douglas, C. M., Pagala, V., Peng, J., Hunt, L. C., Ding, H., Huo, Z., et al. (2024) · JCI Insight · doi:10.1172/jci.insight.174007 · Cited by 31
Self-citationExercise influences circadian gene expression in equine skeletal muscle
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“, 1991), respectively, and are transcriptionally regulated by ARNTL and CLOCK in the skeletal muscle of mice (McCarthy et al., 2007; Andrews et al., 2010) and zebrafish (Amaral and Johnston, 2012).”
BackgroundMetabolic‐sensing of the skeletal muscle clock coordinates fuel oxidation
Yin, H., Li, W., Chatterjee, S., Xiong, X., Saha, P., Yechoor, V. K., & Ma, K. (2020) · The FASEB Journal · doi:10.1096/fj.201903226rr · Cited by 31
Circadian clock genes and respiratory neuroplasticity genes oscillate in the phrenic motor system
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Self-citationExpanding the link between circadian rhythms and redox metabolism of epigenetic control
Sato, T., & Greco, C. M. (2021) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2021.01.009 · Cited by 30
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Time to Train: The Involvement of the Molecular Clock in Exercise Adaptation of Skeletal Muscle
Mansingh, S., & Handschin, C. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2022.902031 · Cited by 29
“The defects in muscle function and structure, and accelerated aging in the BMAL1 KO, were also attributed to loss of MyoD activity (Andrews et al., 2010).”
BackgroundAcute Sleep Deprivation Impairs Motor Inhibition in Table Tennis Athletes: An ERP Study
Xu, L., Song, T., Peng, Z., Dai, C., Wang, L., Shao, Y., Wang, L., Wang, L., & Han, M. (2022) · Brain Sciences · doi:10.3390/brainsci12060746 · Cited by 29
“At the same time, cross-time-zone competition, overly intense competition schedules, increased nighttime competitions, and mood swings such as excitement, tension, and anxiety prior to competition can all interfere with athletes’ circadian and homeostatic rhythms [2,3].”
BackgroundSkeletal muscle gene expression dysregulation in long-term spaceflights and aging is clock-dependent
Malhan, D., Yalçın, M., Schoenrock, B., Blottner, D., & Relógio, A. (2023) · npj Microgravity · doi:10.1038/s41526-023-00273-4 · Cited by 28
“DATA AVAILABILITY The datasets used in this study were retrieved from open-access public repositories and are available as follows: (1) Circadian RNA-seq datasets derived from human skeletal muscle (NCBI-GEO, Accession number: GSE108539, GSE109825), (2) Circadian microarray datasets derived from mouse skeletal muscle…”
MethodThe clock regulator Bmal1 protects against muscular dystrophy
Gao, H., Xiong, X., Lin, Y., Chatterjee, S., & Ma, K. (2020) · Experimental Cell Research · doi:10.1016/j.yexcr.2020.112348 · Cited by 25
Circadian regulation in aging: Implications for spaceflight and life on earth
Malhan, D., Schoenrock, B., Yalçın, M., Blottner, D., & Relógio, A. (2023) · Aging Cell · doi:10.1111/acel.13935 · Cited by 25
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“Gastrocnemius muscles from 30–35-week-old male wild-type and Bmal1−/− (Andrews et al., 2010; Bunger et al., 2000) mice (both n=4) were homogenized using extraction buffer (2% SDS, 10% glycerol, 2% 2-mercaptoethanol, 50 mM Tris-HCl, pH 8.”
BackgroundMethodInfluentialSelf-citationControl of circadian muscle glucose metabolism through the BMAL1–HIF axis in obesity
Chaikin, C., Thakkar, A. V., Steffeck, A. W. T., Pfrender, E. M., Hung, K., Zhu, P., Waldeck, N. J., Nozawa, R., Song, W., Futtner, C. R., et al. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2424046122 · Cited by 29
Aoyama, S., Kojima, S., Sasaki, K., Ishikawa, R., Tanaka, M., Shimoda, T., Hattori, Y., Aoki, N., Takahashi, K., Hirooka, R., et al. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.10.057 · Cited by 23
Zhang, Z., Sinha, J., Bahrami-Nejad, Z., & Teruel, M. N. (2022) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2204470119 · Cited by 22
Nakao, R., Shimba, S., & Oishi, K. (2017) · Scientific Reports · doi:10.1038/s41598-017-03119-8 · Cited by 24
Genome Architecture Mediates Transcriptional Control of Human Myogenic Reprogramming
Liu, S., Chen, H., Ronquist, S., Seaman, L., Ceglia, N., Meixner, W., Chen, P., Higgins, G. A., Baldi, P., Smale, S., et al. (2018) · iScience · doi:10.1016/j.isci.2018.08.002 · Cited by 24
Food deprivation during active phase induces skeletal muscle atrophy via IGF-1 reduction in mice
Abe, T., Kazama, R., Okauchi, H., & Oishi, K. (2019) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2019.108160 · Cited by 25
Cardiolipin Synthesis in Skeletal Muscle Is Rhythmic and Modifiable by Age and Diet
Nohara, K., Kim, E., Wirianto, M., Mileykovskaya, E., Dowhan, W., Chen, Z., & Yoo, S. H. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/5304768 · Cited by 25
“Further, global ClockΔ19 mutation and Bmal1 KO led to impaired muscle structure and physiology, and interestingly, muscle mitochondrial volume and function were found to be strongly attenuated in these mutant mice [21].”
BackgroundWu, P., Li, Y., Cheng, J. R., Chen, L., Zhu, X., Feng, Z., Zhang, J., & Chu, W. (2016) · BMC Genomics · doi:10.1186/s12864-016-3373-z · Cited by 23
“It has been reported that the circadian regulation of myoD expression by lock/arntl was crucial for the skeletal muscle phenotype and function in mouse [32].”
Molecular clocks, satellite cells, and skeletal muscle regeneration
Kahn, R. E., Dayanidhi, S., Lacham‐Kaplan, O., & Hawley, J. A. (2023) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00073.2023 · Cited by 26
From Chronodisruption to Sarcopenia: The Therapeutic Potential of Melatonin
Fernández‐Martínez, J., Ramírez‐Casas, Y., Yang, Y., Aranda‐Martínez, P., Martínez-Ruiz, L., Escames, G., & Acuña-Castroviejo, D. (2023) · Biomolecules · doi:10.3390/biom13121779 · Cited by 22
Circadian control of mitochondrial dynamics and functions
Ezagouri, S., & Asher, G. (2018) · Current Opinion in Physiology · doi:10.1016/j.cophys.2018.05.008 · Cited by 22
“The dependency of mitochondrial morphology on clock genes was corroborated in mouse skeletal muscle [26] and heart [12], and is linked to impaired mitochondrial function in these organs.”
BackgroundMethodCircadian Organelles: Rhythms at All Scales
Aviram, R., Adamovich, Y., & Asher, G. (2021) · Cells · doi:10.3390/cells10092447 · Cited by 22
“Control of mitochondrial morphology by clock genes was also observed in livers from liver-specific Bmal1 knockout mice [74] and from Clock∆19 mice [76] as well as in mouse skeletal muscle and heart [77,78].”
BackgroundRhythms of metabolism in adipose tissue and mitochondria
Onder, Y., & Green, C. B. (2018) · Neurobiology of Sleep and Circadian Rhythms · doi:10.1016/j.nbscr.2018.01.001 · Cited by 22
Budai, Z., Balogh, L., & Sarang, Z. (2019) · International Journal of Food Sciences and Nutrition · doi:10.1080/09637486.2018.1557607 · Cited by 21
“For example, CLOCK or BMAL1 deletion in pancreas results in impaired glucose tolerance and reduced insulin secretion while ablation of the same genes in skeletal muscle leads to the diminished force due to decreased mitochondrial function (Andrews et al. 2010; Marcheva et al. 2010).”
BackgroundIt’s about time: clocks in the developing lung
Bartman, C. M., Matveyenko, A. V., & Prakash, Y. S. (2020) · Journal of Clinical Investigation · doi:10.1172/jci130143 · Cited by 22
“Furthermore, BMAL1-CLOCK regulates myogenesis by transcriptionally targeting the muscle differentiation factor MyoD (83, 84), CRY2 post-transcriptionally regulates myogenic differentiation (85), and REV-ERBα inhibits myogenesis through Wnt (86).”
BackgroundYang, L., Lang, H., Zhou, M., Huang, L., Hui, S., Wang, X., Chen, K., & Mi, M. (2020) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201900991 · Cited by 21
Palm, D., Uzoni, A., Simon, F., Fischer, M., Coogan, A., Tucha, O., Thome, J., & Faltraco, F. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.06.007 · Cited by 20
“mitochondrial biogenesis in human muscle, was altered [78].”
BackgroundMartchenko, S. E., Martchenko, A., Biancolin, A. D., Waller, A. S., & Brubaker, P. L. (2021) · Molecular Metabolism · doi:10.1016/j.molmet.2021.101340 · Cited by 21
CircadiOmics: circadian omic web portal
Samad, M., Agostinelli, F., Sato, T., Shimaji, K., & Baldi, P. (2022) · Nucleic Acids Research · doi:10.1093/nar/gkac419 · Cited by 21
“Consistent with this result, Figure 4 shows that the reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses showed that mRNA and protein W188 Nucleic Acids Research, 2022, Vol. 50 , Web Server issue at ZT 4, 8, 12, 16, 20).”
The skeletal muscle circadian clock regulates titin splicing through RBM20
Riley, L. A., Zhang, X., Douglas, C. M., Mijares, J., Hammers, D. W., Wolff, C. A., Wood, N. B., Olafson, H. R., Du, P., Labeit, S., et al. (2022) · eLife · doi:10.7554/elife.76478 · Cited by 19
Self-citationEffects of light cycle on motion behaviour and melatonin secretion in Haliotis discus hannai
Gao, X., Pang, G., Luo, X., You, W., & Ke, C. (2020) · Aquaculture · doi:10.1016/j.aquaculture.2020.735981 · Cited by 20
BMAL1/PGC1α4-FNDC5/irisin axis impacts distinct outcomes of time-of-day resistance exercise
Guo, M., Shen, F., Guo, X., Zhang, J., Ma, Y., Wu, X., Zuo, H., Yao, J., Hu, Y., Wang, D., et al. (2024) · Journal of sport and health science/Journal of Sport and Health Science · doi:10.1016/j.jshs.2024.100968 · Cited by 21
“17,65 Of note, we noticed an increased MyoD expression in muscles from WT mice trained chronically at LA phase vs. LR phase (Fig.”
Kim, H., Chijiki, H., Fukazawa, M., Okubo, J., Ozaki, M., Nanba, T., Higashi, S., Shioyama, M., Takahashi, M., Nakaoka, T., et al. (2021) · Frontiers in Nutrition · doi:10.3389/fnut.2021.797004 · Cited by 19
“In contrast, it has been reported that the expression of MyoD, a gene involved in muscle differentiation, has a diurnal rhythm controlled by clock genes and is greatly affected by diet (29, 30).”
BackgroundSweeney, H. L., Masiero, S., & Carraro, U. (2022) · European Journal of Translational Myology · doi:10.4081/ejtm.2022.10440 · Cited by 19
NAD+: An old but promising therapeutic agent for skeletal muscle ageing
Xu, Y., & Xiao, W. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102106 · Cited by 20
“An ageing circadian clock exacerbates SMA by inducing metabolic shifts, the loss of proteostasis, mitochondrial dyshomeostasis, and MuSC dysfunction (Andrews et al., 2010; Zhang et al., 2020a).”
Petrenko, V., Saini, C., Perrin, L., & Dibner, C. (2016) · Journal of Visualized Experiments · doi:10.3791/54673 · Cited by 20
Su, Y., Foppen, E., Fliers, E., & Kalsbeek, A. (2016) · Endocrinology · doi:10.1210/en.2016-1083 · Cited by 18
Musculoskeletal Aging and Sarcopenia in the Elderly
Marzetti, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23052808 · Cited by 19
“However, studies in mice lacking CLOCK and BMAL1 have shown that clock gene deficiency causes mitochondrial dysfunction and muscle degeneration [19].”
BackgroundProcopio, S. B., & Esser, K. A. (2024) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2024.11.011 · Cited by 19
Self-citationSteidle‐Kloc, E., Schönfelder, M., Müller, E., Sixt, S., Schuler, G. C., Patsch, W., & Niebauer, J. (2016) · European Journal of Preventive Cardiology · doi:10.1177/2047487316639682 · Cited by 18
“As suggested by Andrews et al.(39) clock genes may generate a muscle-specific circadian transcriptome in an adaptive role for the daily maintenance of adult skeletal muscles and MyoD represents a critical factor for further analysis.”
BackgroundMethodInfluentialMalik, Z. A., Davies, K. A. B., Hall, E. C. R., Barrett, J., Pullinger, S. A., Erskine, R. M., Shepherd, S. O., Iqbal, Z., Edwards, B., & Burniston, J. G. (2020) · Proteomes · doi:10.3390/proteomes8030022 · Cited by 18
“The circadian regulation of this effect is supported by data from animals carrying clock gene mutations that exhibit a decrement in myofiber-specific force and disruption to the hexagonal structure of thick filament proteins [17].”
BackgroundChrono-Nutrition Has Potential in Preventing Age-Related Muscle Loss and Dysfunction
Aoyama, S., Nakahata, Y., & Shinohara, K. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.659883 · Cited by 20
“Similar findings were observed in Clock mutant mice and Rev-erbα knockout mice (Andrews et al., 2010; Mayeuf-Louchart et al., 2017).”
BackgroundResultInfluentialKiriyama, K., Yamamoto, M., Kim, D., Sun, S., Yamamoto, H., & Oda, H. (2022) · British Journal Of Nutrition · doi:10.1017/s0007114522000356 · Cited by 17
“myogenesis and is a circadian oscillator that is regulated by clock genes(56).”
BackgroundCircadian Rhythm in Stroke – The Influence of Our Internal Cellular Clock on Cerebrovascular Events
LeBlanc, N. S. R. (2014) · Journal of Clinical & Experimental Pathology · doi:10.4172/2161-0681.1000163 · Cited by 18
“Mice deficient in Bmal1 suffer from disturbed sleeping behavior, liver and kidney dysfunction [75], metabolic impairment [76], musculosceletal weakness [77], arthritis [78] and eventually premature death [79].”
BackgroundCircadian Rhythm Effects on the Molecular Regulation of Physiological Systems
Crislip, G. R., Johnston, J. G., Douma, L. G., Costello, H. M., Juffre, A., Boyd, K., Li, W. W., Maugans, C. C., Gutierrez‐Monreal, M. A., Esser, K. A., et al. (2021) · Comprehensive physiology · doi:10.1002/cphy.c210011 · Cited by 36
“These studies demonstrated that muscle weakness and mitochondrial deficits were two muscle pathologies common to both genetic mouse models (15).”
Self-citationSutton, E. R., & Pekovic‐Vaughan, V. (2025) · Antioxidants · doi:10.3390/antiox14091132 · Cited by 20
“Bmal1 knock-out (KO) and Clock ∆ 19 mice (with an ablation of exon 19 in the Clock gene) both exhibit ~30% reductions in normalised maximal skeletal muscle force, which is reciprocated at the single-fibre level, with changes in the myofilament architecture impairing contractile ability [66].”
InfluentialMore than the clock: distinct regulation of muscle function and metabolism by PER2 and RORα
Mansingh, S., Maier, G., Delezie, J., Westermark, P. O., Ritz, D., Duchemin, W., Santos, G., Karrer‐Cardel, B., Steurer, S. A., Albrecht, U., et al. (2024) · The Journal of Physiology · doi:10.1113/jp285585 · Cited by 18
“…have been described extensively, including impaired glucose metabolism, insulin resistance and myogenesis, and indicate that ablation of the core clock significantly alters muscle metabolism (Andrews et al., 2010; Dyar et al., 2018; Harfmann et al., 2016; Peek et al., 2017; Perrin et al., 2018).”
The contribution of circadian clock to the biological processes
Luo, B., Song, J., Zhang, J., Han, J., Zhou, X., & Chen, L. (2024) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2024.1387576 · Cited by 17
Metadata
- Authors
- Andrews, J. L., Zhang, X., McCarthy, J. J., McDearmon, E. L., Hornberger, T. A., Russell, B., Campbell, K. S., Arbogast, S., Reid, M. B., Walker, J. R., Hogenesch, J. B., Takahashi, J. S., & Esser, K. A.
- Affiliations
- University of Illinois Chicago (US)
- University of Kentucky (US)
- Northwestern University (US)
- Genomics Institute of the Novartis Research Foundation (US)
- University of Pennsylvania (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-10-18
- Volume
- 107
- Issue
- 44
- Pages
- 19090-19095
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2973897
- OpenAlex
- W2053866174
- Cited by
- 389
- References
- 49
- Citations by year
- 2026: 30 · 2025: 29 · 2024: 31 · 2023: 28 · 2022: 36 · 2021: 26 · 2020: 25 · 2019: 19 · 2018: 27 · 2017: 23 · 2016: 32 · 2015: 20 · 2014: 19 · 2013: 17 · 2012: 15
- FWCI
- 6.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (5p50mh074924-05)
- National Heart, Lung, and Blood Institute (HL45721, R01HL045721)
- National Institute of Mental Health (U01MH061915, P50 MH-074924, U01 MH 61915)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R03AR053641, R21AR050717, AR050717, R01AR055246, AR-053641)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- circadian clock, clocks, Bmal1, MyoD, skeletal muscle, myogenesis, clock-controlled genes, mitochondrial dysfunction, uncoupled respiration, PGC-1α, PGC-1β, muscle force, muscle phenotype
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Gene Expression Regulation, Mice, Inbred BALB C, Mitochondria, Muscle, Transcription Factors, Trans-Activators, MyoD Protein, Mice, Knockout, Muscle, Skeletal, Gene Expression Profiling, Muscle Development, Mice, Electron Microscope Tomography, CLOCK Proteins, ARNTL Transcription Factors, Circadian Clocks
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