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      Circadian regulation in aging: Implications for spaceflight and life on earth

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          Abstract

          Alterations in the circadian system are characteristic of aging on Earth. With the decline in physiological processes due to aging, several health concerns including vision loss, cardiovascular disorders, cognitive impairments, and muscle mass loss arise in elderly populations. Similar health risks are reported as “red flag” risks among astronauts during and after a long‐term Space exploration journey. However, little is known about the common molecular alterations underlying terrestrial aging and space‐related aging in astronauts, and controversial conclusions have been recently reported. In light of the regulatory role of the circadian clock in the maintenance of human health, we review here the overlapping role of the circadian clock both on aging on Earth and spaceflight with a focus on the four most affected systems: visual, cardiovascular, central nervous, and musculoskeletal systems. In this review, we briefly introduce the regulatory role of the circadian clock in specific cellular processes followed by alterations in those processes due to aging. We next summarize the known molecular alterations associated with spaceflight, highlighting involved clock‐regulated genes in space flown Drosophila, nematodes, small mammals, and astronauts. Finally, we discuss common genes that are altered in terms of their expression due to aging on Earth and spaceflight. Altogether, the data elaborated in this review strengthen our hypothesis regarding the timely need to include circadian dysregulation as an emerging hallmark of aging on Earth and beyond.

          Abstract

          Circadian dysregulation as an emerging hallmark of aging on Earth and during space travel.

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          Global prevalence of age-related macular degeneration and disease burden projection for 2020 and 2040: a systematic review and meta-analysis.

          Wan Wong, Xinyi Su, Xiang Li … (2014)
          Numerous population-based studies of age-related macular degeneration have been reported around the world, with the results of some studies suggesting racial or ethnic differences in disease prevalence. Integrating these resources to provide summarised data to establish worldwide prevalence and to project the number of people with age-related macular degeneration from 2020 to 2040 would be a useful guide for global strategies. We did a systematic literature review to identify all population-based studies of age-related macular degeneration published before May, 2013. Only studies using retinal photographs and standardised grading classifications (the Wisconsin age-related maculopathy grading system, the international classification for age-related macular degeneration, or the Rotterdam staging system) were included. Hierarchical Bayesian approaches were used to estimate the pooled prevalence, the 95% credible intervals (CrI), and to examine the difference in prevalence by ethnicity (European, African, Hispanic, Asian) and region (Africa, Asia, Europe, Latin America and the Caribbean, North America, and Oceania). UN World Population Prospects were used to project the number of people affected in 2014 and 2040. Bayes factor was calculated as a measure of statistical evidence, with a score above three indicating substantial evidence. Analysis of 129,664 individuals (aged 30-97 years), with 12,727 cases from 39 studies, showed the pooled prevalence (mapped to an age range of 45-85 years) of early, late, and any age-related macular degeneration to be 8.01% (95% CrI 3.98-15.49), 0.37% (0.18-0.77), and 8.69% (4.26-17.40), respectively. We found a higher prevalence of early and any age-related macular degeneration in Europeans than in Asians (early: 11.2% vs 6.8%, Bayes factor 3.9; any: 12.3% vs 7.4%, Bayes factor 4.3), and early, late, and any age-related macular degeneration to be more prevalent in Europeans than in Africans (early: 11.2% vs 7.1%, Bayes factor 12.2; late: 0.5% vs 0.3%, 3.7; any: 12.3% vs 7.5%, 31.3). There was no difference in prevalence between Asians and Africans (all Bayes factors <1). Europeans had a higher prevalence of geographic atrophy subtype (1.11%, 95% CrI 0.53-2.08) than Africans (0.14%, 0.04-0.45), Asians (0.21%, 0.04-0.87), and Hispanics (0.16%, 0.05-0.46). Between geographical regions, cases of early and any age-related macular degeneration were less prevalent in Asia than in Europe and North America (early: 6.3% vs 14.3% and 12.8% [Bayes factor 2.3 and 7.6]; any: 6.9% vs 18.3% and 14.3% [3.0 and 3.8]). No significant gender effect was noted in prevalence (Bayes factor <1.0). The projected number of people with age-related macular degeneration in 2020 is 196 million (95% CrI 140-261), increasing to 288 million in 2040 (205-399). These estimates indicate the substantial global burden of age-related macular degeneration. Summarised data provide information for understanding the effect of the condition and provide data towards designing eye-care strategies and health services around the world. National Medical Research Council, Singapore. Copyright © 2014 Wong et al. Open Access article distributed under the terms of CC BY-NC-ND. Published by .. All rights reserved.
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            Hallmarks of aging: An expanding universe

            Carlos López-Otín, Maria Blasco, Linda Partridge … (2023)
            Aging is driven by hallmarks fulfilling the following three premises: (1) their age-associated manifestation, (2) the acceleration of aging by experimentally accentuating them, and (3) the opportunity to decelerate, stop, or reverse aging by therapeutic interventions on them. We propose the following twelve hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. These hallmarks are interconnected among each other, as well as to the recently proposed hallmarks of health, which include organizational features of spatial compartmentalization, maintenance of homeostasis, and adequate responses to stress.
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              A circadian gene expression atlas in mammals: implications for biology and medicine.

              Ray Zhang, Nicholas Lahens, Heather I Ballance … (2014)
              To characterize the role of the circadian clock in mouse physiology and behavior, we used RNA-seq and DNA arrays to quantify the transcriptomes of 12 mouse organs over time. We found 43% of all protein coding genes showed circadian rhythms in transcription somewhere in the body, largely in an organ-specific manner. In most organs, we noticed the expression of many oscillating genes peaked during transcriptional "rush hours" preceding dawn and dusk. Looking at the genomic landscape of rhythmic genes, we saw that they clustered together, were longer, and had more spliceforms than nonoscillating genes. Systems-level analysis revealed intricate rhythmic orchestration of gene pathways throughout the body. We also found oscillations in the expression of more than 1,000 known and novel noncoding RNAs (ncRNAs). Supporting their potential role in mediating clock function, ncRNAs conserved between mouse and human showed rhythmic expression in similar proportions as protein coding genes. Importantly, we also found that the majority of best-selling drugs and World Health Organization essential medicines directly target the products of rhythmic genes. Many of these drugs have short half-lives and may benefit from timed dosage. In sum, this study highlights critical, systemic, and surprising roles of the mammalian circadian clock and provides a blueprint for advancement in chronotherapy.
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                Author and article information

                Contributors
                Angela Relόgio: angela.relogio@medicalschool-hamburg.de
                Journal
                Journal ID (nlm-ta): Aging Cell
                Journal ID (iso-abbrev): Aging Cell
                Journal ID (doi): 10.1111/(ISSN)1474-9726
                Journal ID (publisher-id): ACEL
                Title: Aging Cell
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1474-9718
                ISSN (Electronic): 1474-9726
                Publication date (Electronic): 26 July 2023
                Publication date Collection: September 2023
                Volume: 22
                Issue: 9 ( doiID: 10.1111/acel.v22.9 )
                Electronic Location Identifier: e13935
                Affiliations
                [ 1 ] Institute for Systems Medicine and Faculty of Human Medicine MSH Medical School Hamburg Hamburg Germany
                [ 2 ] Institute of Integrative Neuroanatomy Charité‐Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health Berlin Germany
                [ 3 ] Institute for Theoretical Biology (ITB) Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health Berlin Germany
                [ 4 ] Molecular Cancer Research Center (MKFZ), Medical Department of Hematology, Oncology, and Tumour Immunology, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health Berlin Germany
                [ 5 ] Neuromuscular System and Neuromuscular Signaling Berlin Center of Space Medicine & Extreme Environments Berlin Germany
                Author notes
                [*] [* ] Correspondence

                Angela Relόgio, Institute for Systems Medicine and Faculty of Human Medicine, MSH Medical School Hamburg, Hamburg 20457, Germany.

                Email: angela.relogio@ 123456medicalschool-hamburg.de

                Author information
                https://orcid.org/0000-0002-5634-3833
                Article
                Publisher ID: ACEL13935 Other ID: ACE-23-0341-R.R1
                DOI: 10.1111/acel.13935
                PMC ID: 10497835
                PubMed ID: 37493006
                SO-VID: a04a1377-7cd0-41af-aa30-b031b37871ac
                Copyright © © 2023 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date revision received : 30 June 2023
                Date received : 08 May 2023
                Date accepted : 07 July 2023
                Page count
                Figures: 4, Tables: 2, Pages: 23, Words: 17034
                Funding
                Funded by: Deutsches Zentrum für Luft‐ und Raumfahrt
                Award ID: #50WB2029
                Funded by: Dr. Rolf M. Schwiete Stiftung , doi 10.13039/501100020027;
                Categories
                Subject: Review Article
                Subject: Review Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date September 2023
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.3 mode:remove_FC converted:13.09.2023

                ScienceOpen disciplines: Cell biology
                Keywords: aging,biological aging,circadian clock,circadian rhythms,space exploration,spaceflight
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: aging, biological aging, circadian clock, circadian rhythms, space exploration, spaceflight

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