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Cited by 219Circadian rhythm and melatoninMitochondrial Function and PathologySleep and Work-Related Fatigue

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Circadian rhythms in mitochondrial respiration

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de Goede, Paul, Wefers, Jakob, Brombacher, Eline Constance, Schrauwen, Patrick, Kalsbeek, Andries·2018·Journal of Molecular Endocrinology
DOI 10.1530/jme-17-0196PMC PMC5854864
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Abstract

Many physiological processes are regulated with a 24-h periodicity to anticipate the environmental changes of daytime to nighttime and vice versa. These 24-h regulations, commonly termed circadian rhythms, among others control the sleep-wake cycle, locomotor activity and preparation for food availability during the active phase (daytime for humans and nighttime for nocturnal animals). Disturbing circadian rhythms at the organ or whole-body level by social jetlag or shift work, increases the risk to develop chronic metabolic diseases such as type 2 diabetes mellitus. The molecular basis of this risk is a topic of increasing interest. Mitochondria are essential organelles that produce the majority of energy in eukaryotes by converting lipids and carbohydrates into ATP through oxidative phosphorylation. To adapt to the ever-changing environment, mitochondria are highly dynamic in form and function and a loss of this flexibility is linked to metabolic diseases. Interestingly, recent studies have indicated that changes in mitochondrial morphology (i.e., fusion and fission) as well as generation of new mitochondria are dependent on a viable circadian clock. In addition, fission and fusion processes display diurnal changes that are aligned to the light/darkness cycle. Besides morphological changes, mitochondrial respiration also displays diurnal changes. Disturbing the molecular clock in animal models leads to abrogated mitochondrial rhythmicity and altered respiration. Moreover, mitochondrial-dependent production of reactive oxygen species, which plays a role in cellular signaling, has also been linked to the circadian clock. In this review, we will summarize recent advances in the study of circadian rhythms of mitochondria and how this is linked to the molecular circadian clock.

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Figure 1 The molecular circadian clock and tissue-specific clocks in the body. CLOCK and BMAL1 form a heterodimer that binds to E-box regulatory sequences PER/CRY and other genes. PER and CRY form a repressor complex, which inhibitsCLOCK-BMAL1 when sufficient levels are reached. The second feedback loop involves nuclear orphan receptors, which bind to the retinoic acid-related orphan receptor response elements (ROREs) in CLOCK and BMAL1 regulatory sequences. Retinoid-related orphan receptor (ROR) activates transcription of CLOCK and BMAL1. The CLOCK-BMAL1 complex induces transcription of REVERBA and REVERBB (REV), which subsequently compete with ROR, in order to inhibit transcription of CLOCK and BMAL1. Circadian clocks exist in almost every cell and exhibit tissue-specific rhythmicity, orchestrated by the central circadian clock in the suprachiasmatic nucleus. Synchronization takes place via neural, hormonal and behavioral signals.
Figure 1 The molecular circadian clock and tissue-specific clocks in the body. CLOCK and BMAL1 form a heterodimer that binds to E-box regulatory sequences PER/CRY and other genes. PER and CRY form a repressor complex, which inhibitsCLOCK-BMAL1 when sufficient levels are reached. The second feedback loop involves nuclear orphan receptors, which bind to the retinoic acid-related orphan receptor response elements (ROREs) in CLOCK and BMAL1 regulatory sequences. Retinoid-related orphan receptor (ROR) activates transcription of CLOCK and BMAL1. The CLOCK-BMAL1 complex induces transcription of REVERBA and REVERBB (REV), which subsequently compete with ROR, in order to inhibit transcription of CLOCK and BMAL1. Circadian clocks exist in almost every cell and exhibit tissue-specific rhythmicity, orchestrated by the central circadian clock in the suprachiasmatic nucleus. Synchronization takes place via neural, hormonal and behavioral signals.CC BY · PubMed Central
Figure 2 Model for circadian regulation of mitochondrial homeostasis. To maintain healthy mitochondria, mitochondria are continuously formed and removed during the active phase. The CLOCK-BMAL1 complex stimulates mitochondrial biogenesis and mitophagy through activation of SIRT1. Mitochondrial biogenesis is regulated by transcription factor PGC1A. Newly formed mitochondria fuse to form a tubular network. Mitophagy is preceded by mitochondrial fission in order to form fragmented mitochondria which can be taken up by an autophagosome. Both fusion and fission are influenced by CLOCK-BMAL1. A number of regulatory proteins regulate fusion (OPA1, MFN1/2), fission (FIS1, DRP1) and mitophagy (PINK1, BNIP1, PARKIN) processes.
Figure 2 Model for circadian regulation of mitochondrial homeostasis. To maintain healthy mitochondria, mitochondria are continuously formed and removed during the active phase. The CLOCK-BMAL1 complex stimulates mitochondrial biogenesis and mitophagy through activation of SIRT1. Mitochondrial biogenesis is regulated by transcription factor PGC1A. Newly formed mitochondria fuse to form a tubular network. Mitophagy is preceded by mitochondrial fission in order to form fragmented mitochondria which can be taken up by an autophagosome. Both fusion and fission are influenced by CLOCK-BMAL1. A number of regulatory proteins regulate fusion (OPA1, MFN1/2), fission (FIS1, DRP1) and mitophagy (PINK1, BNIP1, PARKIN) processes.CC BY · PubMed Central
Figure 3 Mitochondrial respiration and ROS production show rhythmic activity. Mitochondrial respiration is the result of electron transfer to molecular oxygen as final step in the electron transport chain (ETC). Respiration is experimentally determined by measuring OCR. In addition, 14C-labeled substrates can be used to assess mitochondrial energy production by measuring 14CO2. Substrate transport (CPT1/2, PDH) and catabolic processes (β-oxidation, TCA cycle) also exhibit circadian rhythms and are under control of the circadian clock. Consequently, mitochondrial respiration is rhythmic in various cell and animal models. Mitochondria are also a source of ROS that are produced in various sites, such as complex I of the ETC. Superoxides (O2 −) are scavenged by superoxidedismutase (SOD) and reduced to H2O2. Several antioxidant proteins such as peroxiredoxins (PRXIII) subsequently eliminate H2O2. Also antioxidant proteins and ROS production display circadian activity. Additionally, feeding behavior, including diet composition, also affects mitochondrial processes.
Figure 3 Mitochondrial respiration and ROS production show rhythmic activity. Mitochondrial respiration is the result of electron transfer to molecular oxygen as final step in the electron transport chain (ETC). Respiration is experimentally determined by measuring OCR. In addition, 14C-labeled substrates can be used to assess mitochondrial energy production by measuring 14CO2. Substrate transport (CPT1/2, PDH) and catabolic processes (β-oxidation, TCA cycle) also exhibit circadian rhythms and are under control of the circadian clock. Consequently, mitochondrial respiration is rhythmic in various cell and animal models. Mitochondria are also a source of ROS that are produced in various sites, such as complex I of the ETC. Superoxides (O2 −) are scavenged by superoxidedismutase (SOD) and reduced to H2O2. Several antioxidant proteins such as peroxiredoxins (PRXIII) subsequently eliminate H2O2. Also antioxidant proteins and ROS production display circadian activity. Additionally, feeding behavior, including diet composition, also affects mitochondrial processes.CC BY · PubMed Central

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Research works printed but not linked: 89

  1. 2012, Feedback control of adrenal steroidogenesis via H2O2-dependent, reversible inactivation of peroxiredoxin III in mitochondria, Molecular Cell, 46, 584, 10.1016/j.molcel.2012.05.030 · DOI
  2. 2002, The role of maternal mitochondria during oogenesis, fertilization and embryogenesis, Reproductive BioMedicine Online, 4, 176, 10.1016/S1472-6483(10)61937-2 · DOI
  3. 2011, Temporal orchestration of circadian autophagy rhythm by C/EBPβ, EMBO Journal, 30, 4642, 10.1038/emboj.2011.322 · DOI · Paper page
  4. 2016, Clock genes-dependent acetylation of complex I sets rhythmic activity of mitochondrial OxPhos, Biochimica et Biophysica Acta (BBA): Molecular Cell Research, 1863, 596, 10.1016/j.bbamcr.2015.12.018 · DOI
  5. 2014, Crosstalk between circadian rhythmicity, mitochondrial dynamics and macrophage bactericidal activity, Immunology, 143, 490, 10.1111/imm.12329 · DOI
  6. 2017, Differential effects of diet composition and timing of feeding behavior on rat brown adipose tissue and skeletal muscle peripheral clocks, Neurobiology of Sleep and Circadian Rhythms, 4, 24
  7. 1999, Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1, Cell, 98, 115, 10.1016/S0092-8674(00)80611-X · DOI · Paper page
  8. 2015, Acute and delayed responses of C-reactive protein, malondialdehyde and antioxidant markers after resistance training session in elite weightlifters: effect of time of day, Chronobiology International, 32, 1211, 10.3109/07420528.2015.1079215 · DOI
  9. 2009, Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis, Science, 324, 651, 10.1126/science.1171641 · DOI · Paper page
  10. 2011, Uncoupling proteins and the control of mitochondrial reactive oxygen species production, Free Radical Biology and Medicine, 51, 1106, 10.1016/j.freeradbiomed.2011.06.022 · DOI
  11. 2003, The molecular machinery of Keilin’s respiratory chain, Biochemical Society Transactions, 31, 1095, 10.1042/bst0311095 · DOI
  12. 2017, Circadian and feeding rhythms orchestrate the diurnal liver acetylome, Cell Reports, 20, 1729, 10.1016/j.celrep.2017.07.065 · DOI
  13. 1979, Neonatal suprachiasmatic nucleus lesions: effects on the development of circadian rhythms in the rat, Brain Research, 164, 17, 10.1016/0006-8993(79)90003-9 · DOI
  14. 2012, Peroxiredoxins are conserved markers of circadian rhythms, Nature, 485, 459, 10.1038/nature11088 · DOI
  15. 2009, Nicotinamide enhances mitochondria quality through autophagy activation in human cells, Aging Cell, 8, 426, 10.1111/j.1474-9726.2009.00487.x · DOI
  16. YBuggerHZhangD, 2008, Disruption of the circadian clock within the cardiomyocyte influences myocardial contractile function metabolism and gene expression of : and, American Journal Physiology Heart Circulatory Physiology, 294
  17. 2014, The circadian clock maintains cardiac function by regulating mitochondrial metabolism in mice, PLoS ONE, 9, e112811, 10.1371/journal.pone.0112811 · DOI
  18. 2017, CRY1/2 selectively repress PPARδ and limit exercise capacity, Cell Metabolism, 26, 243.e6
  19. 2015, The endogenous molecular clock orchestrates the temporal separation of substrate metabolism in skeletal muscle., Skeletal Muscle, 5, 17, 10.1186/s13395-015-0039-5 · DOI
  20. 2015, The mammalian circadian clock gene Per2 modulates cell death in response to oxidative stress, Frontiers in Neurology, 5, 289
  21. 2001, Regulation of clock and NPAS2 DNA binding by the redox state of NAD cofactors, Science, 293, 510, 10.1126/science.1060698 · DOI · Paper page
  22. Neufeld, 2016, NooriLKupermanYGolikM Circadian control of oscillations in mitochondrial rate - limiting enzymes and nutrient utilization by PERIOD proteins https org, 113, 10.1073/pnas.1519650113 · DOI · Paper page
  23. 2012, Circadian autophagy rhythm: a link between clock and metabolism?, Trends in Endocrinology and Metabolism, 23, 319, 10.1016/j.tem.2012.03.004 · DOI
  24. 2016, Clock-genes and mitochondrial respiratory activity: evidence of a reciprocal interplay, Biochimica et Biophysica Acta (BBA): Bioenergetics, 1857, 1344, 10.1016/j.bbabio.2016.03.035 · DOI
  25. 2016, Mitochondrial H2O2 signaling is controlled by the concerted action of peroxiredoxin III and sulfiredoxin: linking mitochondrial function to circadian rhythm, Free Radical Biology and Medicine, 100, 73, 10.1016/j.freeradbiomed.2016.10.011 · DOI
  26. 2014b, Liver Clock Protein BMAL1 Promotes de Novo Lipogenesis through Insulin-mTORC2-AKT Signalling, Journal of Biological Chemistry, 289, 25925, 10.1074/jbc.M114.567628 · DOI
  27. 1993, Surviving Hypoxia: Mechanisms of Control and Adaptation
  28. 2003, Circadian rhythms of oxidative phosphorylation: effects of rotenone and melatonin on isolated rat brain mitochondria, Chronobiology International, 20, 451, 10.1081/CBI-120021385 · DOI
  29. 2009, Proteome differences between brown and white fat mitochondria reveal specialized metabolic functions, Cell Metabolism, 10, 324, 10.1016/j.cmet.2009.08.014 · DOI
  30. 2005, Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1, Nature, 434, 113, 10.1038/nature03354 · DOI · Paper page
  31. 2015, Molecular mechanisms of mitochondrial autophagy/mitophagy in the heart, Circulation Research, 116, 1477, 10.1161/CIRCRESAHA.116.303790 · DOI
  32. 2015, The daily rhythms of mitochondrial gene expression and oxidative stress regulation are altered by aging in the mouse liver, Chronobiology International, 32, 1254, 10.3109/07420528.2015.1085388 · DOI
  33. 2015, Response of peripheral rhythms to the timing of food intake, Methods in Enzymology, 552, 145, 10.1016/bs.mie.2014.10.027 · DOI
  34. 1974, Proceedings: diurnal variation in athletic performance, Journal of Physiology, 236, 51P
  35. 2015, In vivo single-cell detection of metabolic oscillations in stem cells, Cell Reports, 10, 1, 10.1016/j.celrep.2014.12.007 · DOI
  36. 2015, ROS-dependent signal transduction, Current Opinion in Cell Biology, 33, 8, 10.1016/j.ceb.2014.09.010 · DOI
  37. 1998, Light responsiveness of the suprachiasmatic nucleus: long-term multiunit and single-unit recordings in freely moving rats, Journal of Neuroscience, 18, 9078, 10.1523/JNEUROSCI.18-21-09078.1998 · DOI
  38. 1981, Autophagic vacuoles in heart muscle and liver. A comparative morphometric study including circadian variations in meal-fed rats, Journal of Molecular and Cellular Cardiology, 13, 37, 10.1016/0022-2828(81)90227-3 · DOI
  39. 2008, The NAD+-dependent deacetylase SIRT1 modulates CLOCK-mediated chromatin remodeling and circadian control, Cell, 134, 329, 10.1016/j.cell.2008.07.002 · DOI · Paper page
  40. 2012, Nicotinamide-induced Mitophagy, Journal of Biological Chemistry, 287, 19304, 10.1074/jbc.M112.363747 · DOI
  41. 1984, Circadian rhythms in multiple unit activity inside and outside the suprachiasmatic nucleus in the diurnal chipmunk (Eutamias sibiricus), Neuroscience Research, 1, 45, 10.1016/0168-0102(84)90029-4 · DOI
  42. 2006, How might you compare mitochondria from different tissues and different species?, Journal of Comparative Physiology B, 176, 93, 10.1007/s00360-005-0025-z · DOI
  43. 2008, In vivo monitoring of circadian timing in freely moving mice, Current Biology, 18, 381, 10.1016/j.cub.2008.02.024 · DOI
  44. 2014, A circadian gene expression atlas in mammals: implications for biology and medicine, PNAS, 111, 16219, 10.1073/pnas.1408886111 · DOI · Paper page
  45. 2016, The evolution of per-cell organelle number, Frontiers in Cell and Developmental Biology, 4, 85
  46. 2015, Hepatic Bmal1 regulates rhythmic mitochondrial dynamics and promotes metabolic fitness, Cell Metabolism, 22, 709, 10.1016/j.cmet.2015.08.006 · DOI
  47. 2011, Tubular network formation protects mitochondria from autophagosomal degradation during nutrient starvation, PNAS, 108, 10190, 10.1073/pnas.1107402108 · DOI
  48. 2008, SIRT1 regulates circadian clock gene expression through PER2 deacetylation, Cell, 134, 317, 10.1016/j.cell.2008.06.050 · DOI · Paper page
  49. 2011, Loss of Bmal1 leads to uncoupling and impaired glucose-stimulated insulin secretion in β-cells, Islets, 3, 381, 10.4161/isl.3.6.18157 · DOI
  50. 2013, Circadian clock NAD+ cycle drives mitochondrial oxidative metabolism in mice, Science, 342, 1243417, 10.1126/science.1243417 · DOI
  51. 2012, Physiological roles of mitochondrial reactive oxygen species, Molecular Cell, 48, 158, 10.1016/j.molcel.2012.09.025 · DOI · Paper page
  52. 2011, During autophagy mitochondria elongate, are spared from degradation and sustain cell viability, Nature Cell Biology, 13, 589, 10.1038/ncb2220 · DOI · Paper page
  53. 2012, Mitophagy: mechanisms, pathophysiological roles, and analysis, Biological Chemistry, 393, 547, 10.1515/hsz-2012-0119 · DOI · Paper page
  54. ChenHChanDC, 2009, Mitochondrial dynamics fusion fission movement and mitophagy in neurodegenerative diseases https org, Human Molecular Genetics, 18, 169, 10.1093/hmg/ddp326 · DOI
  55. 1998, Inter-tissue differences in mitochondrial enzyme activity, RNA and DNA in rainbow trout (Oncorhynchus mykiss), Journal of Experimental Biology, 201, 3377, 10.1242/jeb.201.24.3377 · DOI
  56. 2013, Rev-erb-α modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy, Nature Medicine, 19, 1039, 10.1038/nm.3213 · DOI
  57. 2013, Mitochondrial morphology in mitophagy and macroautophagy, Biochimica et Biophysica Acta (BBA): Molecular Cell Research, 1833, 205, 10.1016/j.bbamcr.2012.02.012 · DOI
  58. 2015, Circadian oscillation of sulfiredoxin in the mitochondria, Molecular Cell, 59, 651, 10.1016/j.molcel.2015.06.031 · DOI
  59. 2015, Teaching the fundamentals of electron transfer reactions in mitochondria and the production and detection of reactive oxygen species, Redox Biology, 4, 381, 10.1016/j.redox.2015.02.001 · DOI
  60. 2012, Transcriptional architecture and chromatin landscape of the core circadian clock in mammals, Science, 338, 349, 10.1126/science.1226339 · DOI · Paper page
  61. 2006, Dissecting the functions of the mammalian clock protein BMAL1 by tissue-specific rescue in mice, Science, 314, 1304, 10.1126/science.1132430 · DOI
  62. 2015, The impact of circadian phenotype and time since awakening on diurnal performance in athletes, Current Biology, 25, 518, 10.1016/j.cub.2014.12.036 · DOI
  63. 2016, Circadian oscillations of NADH redox state using a heterologous metabolic sensor in mammalian cells, Journal of Biological Chemistry, 291, 23906, 10.1074/jbc.M116.728774 · DOI
  64. 2007, Identification of the circadian transcriptome in adult mouse skeletal muscle, Physiological Genomics, 31, 86, 10.1152/physiolgenomics.00066.2007 · DOI
  65. 2002, Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres, Nature, 418, 797, 10.1038/nature00904 · DOI · Paper page
  66. 1975, A morphometric study of cellular autophagy including diurnal variations in kidney tubules of normal rats, Journal of Cell Biology, 64, 608, 10.1083/jcb.64.3.608 · DOI
  67. 2008, Mitochondrial biogenesis and turnover, Cell Calcium, 44, 24, 10.1016/j.ceca.2007.12.004 · DOI
  68. 2017, Mitochondrial dynamics: coupling mitochondrial fitness with healthy aging, Trends in Molecular Medicine, 23, 201, 10.1016/j.molmed.2017.01.003 · DOI
  69. 2004, Evidence for mitochondrial thioesterase as a peroxisome proliferator - activated receptor - α - regulated gene in cardiac and skeletal muscle of and https org, American Journal Physiology Endocrinology Metabolism, 1, 10.1152/ajpendo.00190.2004 · DOI
  70. 2015, Mitochondrial dynamics and mitochondrial quality control, Redox Biology, 4, 6, 10.1016/j.redox.2014.11.006 · DOI · Paper page
  71. 2007, Transcriptional coactivator PGC-1alpha integrates the mammalian clock and energy metabolism, Nature, 447, 477, 10.1038/nature05767 · DOI · Paper page
  72. 2014, Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock, Molecular Metabolism, 3, 29, 10.1016/j.molmet.2013.10.005 · DOI · Paper page
  73. 2005, Metabolic control through the PGC-1 family of transcription coactivators, Cell Metabolism, 1, 361, 10.1016/j.cmet.2005.05.004 · DOI · Paper page
  74. 2011, Mechanisms of mitophagy, Nature Reviews Molecular Cell Biology, 12, 9, 10.1038/nrm3028 · DOI · Paper page
  75. 2008, Fission and selective fusion govern mitochondrial segregation and elimination by autophagy, EMBO Journal, 27, 433, 10.1038/sj.emboj.7601963 · DOI · Paper page
  76. 2010, CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function, PNAS, 107, 19090, 10.1073/pnas.1014523107 · DOI · Paper page
  77. 2002, Coordinated transcription of key pathways in the mouse by the circadian clock, Cell, 109, 307, 10.1016/S0092-8674(02)00722-5 · DOI
  78. 2012, Diurnal variation of hepatic antioxidant gene expression in mice, PLoS ONE, 7, e44237, 10.1371/journal.pone.0044237 · DOI
  79. 2016, Demonstration of a day-night rhythm in human skeletal muscle oxidative capacity, Molecular Metabolism, 5, 635, 10.1016/j.molmet.2016.06.012 · DOI · Paper page
  80. 2009, Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1, Science, 324, 654, 10.1126/science.1170803 · DOI · Paper page
  81. 2016, Mitochondrial dynamics and metabolic regulation, Trends in Endocrinology and Metabolism, 27, 105, 10.1016/j.tem.2015.12.001 · DOI
  82. MHoodDA, 2003, coactivator alpha expression during thyroid hormone - and contractile activity - induced mitochondrial adaptations of https org, American Journal Physiology Cell Physiology, 1, 10.1152/ajpcell.00409.2002 · DOI
  83. 2010, Regulation of mitochondrial biogenesis, Essays in Biochemistry, 47, 69, 10.1042/bse0470069 · DOI · Paper page
  84. 2013, Mitochondrial fission-fusion as an emerging key regulator of cell proliferation and differentiation, BioEssays, 35, 955, 10.1002/bies.201300011 · DOI
  85. 2006, Quantitative proteomic comparison of rat mitochondria from muscle, heart, and liver, Molecular and Cellular Proteomics, 5, 608, 10.1074/mcp.M500298-MCP200 · DOI
  86. 2011, Genome-wide and phase-specific DNA-binding rhythms of BMAL1 control circadian output functions in mouse liver, PLoS Biology, 9, e1000595, 10.1371/journal.pbio.1000595 · DOI
  87. 2016, The circadian gene Rev-erbα improves cellular bioenergetics and provides preconditioning for protection against oxidative stress, Free Radical Biology and Medicine, 93, 177, 10.1016/j.freeradbiomed.2016.02.004 · DOI
  88. 2011, Tissue-specific differences in mitochondrial activity and biogenesis, Mitochondrion, 11, 207, 10.1016/j.mito.2010.09.011 · DOI
  89. 2015, Circadian regulation of cellular physiology, Methods in Enzymology, 552, 165, 10.1016/bs.mie.2014.10.006 · DOI · Paper page

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Authors
de Goede, P., Wefers, J., Brombacher, E. C., Schrauwen, P., & Kalsbeek, A.
Affiliations
  • 1Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands
  • Maastricht University Medical Centre (NL)
  • Amsterdam UMC Location University of Amsterdam (NL)
  • Netherlands Institute for Neuroscience (NL)
Corresponding author
Kalsbeek, Andries
ORCID
Venue
Journal of Molecular Endocrinology
Publisher
Bioscientifica
Published
2018-04
Volume
60
Issue
3
Pages
R115-R130
ISSN
  • 0952-5041 (ISSN-L)
  • 1479-6813
DOI
10.1530/jme-17-0196
PMC
PMC5854864
OpenAlex
W2789456434
Cited by
211
References
91
Citations by year
2026: 24 · 2025: 31 · 2024: 27 · 2023: 30 · 2022: 30 · 2021: 22 · 2020: 26 · 2019: 13 · 2018: 8
FWCI
2.41
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Molecular Endocrinology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • KNAW research portal (Royal Academy of Art and Sciences (KNAW)) (publishedVersion, other-oa)
  • Pure Amsterdam UMC (submittedVersion, other-oa)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
  • Research Publications (Maastricht University) (submittedVersion, cc-by)
  • Research Publications (Maastricht University) (submittedVersion, other-oa)
Funders
Nederlandse Organisatie voor Wetenschappelijk Onderzoek (40-00812-98-1404, 40-00812-98-14047)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
circadian rhythm, mitochondrial respiration, circadian clock, mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, mitochondrial biogenesis, oxidative phosphorylation, reactive oxygen species, type 2 diabetes, metabolic disorders, shift work, social jetlag, light-dark cycle
MeSH terms
Animals, Circadian Rhythm, Humans, Mitochondria, Models, Biological, Reactive Oxygen Species, Cell Respiration, Mitophagy

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