Evidence map›Paper›PMID 25642238›Full record

ReviewFrontiers in genetics2014

The aging clock and circadian control of metabolism and genome stability.

Victoria P Belancio, David E Blask, Prescott Deininger, Steven M Hill, S Michal Jazwinski

Abstract readReview
In one paragraph

Review in Frontiers in genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. How does healthy aging impact on the circadian clock?Journal of neural transmission (Vienna, Austria : 1996) · 2017
    Review
  13. Article
  14. Article
  15. Review
  16. How retrotransposons shape genome regulation.Current opinion in genetics & development · 2016
    Review
  17. Article
  18. Article
  19. The Circadian NADBioMed research international · 2016
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Victoria P BelancioDepartment of Structural and Cellular Biology, Tulane School of Medicine, Tulane University New Orleans, LA, USA ; Tulane Cancer Center, Tulane Center for Aging, and Tulane Center for Circadian Biology New Orleans, LA, USA.
David E BlaskDepartment of Structural and Cellular Biology, Tulane School of Medicine, Tulane University New Orleans, LA, USA ; Tulane Cancer Center, Tulane Center for Aging, and Tulane Center for Circadian Biology New Orleans, LA, USA.
Prescott DeiningerTulane Cancer Center, Tulane Center for Aging, and Tulane Center for Circadian Biology New Orleans, LA, USA ; Department of Epidemiology, Tulane University New Orleans, LA, USA.
Steven M HillDepartment of Structural and Cellular Biology, Tulane School of Medicine, Tulane University New Orleans, LA, USA ; Tulane Cancer Center, Tulane Center for Aging, and Tulane Center for Circadian Biology New Orleans, LA, USA.
S Michal JazwinskiTulane Cancer Center, Tulane Center for Aging, and Tulane Center for Circadian Biology New Orleans, LA, USA ; Department of Medicine, Tulane University New Orleans, LA, USA.

Funding

CELLULAR AGING IN A YEAST MODEL SYSTEMR37AG006168 · NIA · TULANE UNIVERSITY OF LOUISIANA · PI JAZWINSKI, S MICHAL · 1994 to 2016
$5.0M
Mentoring a Cancer Genetics ProgramP20GM103518 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 2012 to 2013
$4.3M
Sine RetrotranspositionR01GM045668 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 1993 to 2014
$4.2M
NIA NIH HHS R37 AG006168NIGMS NIH HHS P20 GM103518NIGMS NIH HHS R01 GM045668
6 · The paper itself

Abstract

It is widely accepted that aging is characterized by a gradual decline in the efficiency and accuracy of biological processes, leading to deterioration of physiological functions and development of age-associated diseases. Age-dependent accumulation of genomic instability and development of metabolic syndrome are well-recognized components of the aging phenotype, both of which have been extensively studied. Existing findings strongly support the view that the integrity of the cellular genome and metabolic function can be influenced by light at night (LAN) and associated suppression of circadian melatonin production. While LAN is reported to accelerate aging by promoting age-associated carcinogenesis in several animal models, the specific molecular mechanism(s) of its action are not fully understood. Here, we review literature supporting a connection between LAN-induced central circadian disruption of peripheral circadian rhythms and clock function, LINE-1 retrotransposon-associated genomic instability, metabolic deregulation, and aging. We propose that aging is a progressive decline in the stability, continuity, and synchronization of multi-frequency oscillations in biological processes to a temporally disorganized state. By extension, healthy aging is the ability to maintain the most consistent, stable, and entrainable rhythmicity and coordination of these oscillations, at the molecular, cellular, and systemic levels.

Indexed as

aginglight exposure at nightLINE-1metabolismretroelements

Identifiers

PMID25642238
PMCPMC4294216

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.