Evidence map›Paper›PMID 22109832›Full record

ArticleAge (Dordrecht, Netherlands)2013

Aging and vascular dysfunction: beneficial melatonin effects.

Luigi Fabrizio Rodella, Gaia Favero, Claudia Rossini, Eleonora Foglio, Francesca Bonomini, Russel J Reiter, Rita Rezzani

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Age (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% of its field
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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  7. Article
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  10. Article
  11. Article
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  13. Article
  14. Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks.International journal of molecular sciences · 2019
    Review
  15. Sirtuins and NADCirculation research · 2018
    Review
  16. Article
  17. Article
  18. Review
  19. Article
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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

7 authors at 3 institutions in 2 countries.

Luigi Fabrizio RodellaDepartment of Biomedical Sciences and Biotechnologies, Section of Human Anatomy, University of Brescia, Viale Europa 11, Brescia, Italy.
Gaia Favero
Claudia Rossini
Eleonora Foglio
Francesca Bonomini
Russel J Reiter
Rita Rezzani
Brescia University · USUniversity of Brescia · ITThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is characterized by a progressive deterioration of physiological functions and metabolic processes. In aging and in diseases associated with the elderly, the loss of cells in vital structures or organs may be related to several factors. Sirtuin1 (SIRT1) is a member of the sirtuin family of protein deacetylases involved in life span extension; however, its involvement in the aging is not yet completely defined. Recently, melatonin, a pleiotropic molecule, shown to activate SIRT1 in primary neurons of young animals, as well as in aged neurons of a murine model of senescence. Melatonin is known to modulate oxidative stress-induced senescence and pro-survival pathways. We treated 6- and 15-week-old apolipoprotein E (APOE)-deficient mice (APOE 6w and 15w) with two melatonin formulations (FAST and RETARD) to evaluate their anti-aging effect. Morphological changes in vessels (aortic arch) of APOE mice were evaluated SIRT1, p53, endothelial nitric oxide synthase (eNOS), and endothelin-1 (ET-1) markers. We demonstrate that SIRT1 and eNOS decresed in APOE mice between 6 and 15 weeks and that aging induced an elevated expression of p53 and ET-1 in APOE animals. Melatonin improved the impairment of endothelial damage and reduced loss of SIRT1 and eNOS decreasing p53 and ET-1 expression. The RETARD melatonin preparation caused a greater improvement of vessel cytoarchitecture. In summary, we indicate that SIRT1-p53-eNOS axis as one of the important marker of advanced vascular dysfunctions linked to aging. Finally, we suggest that extended-release melatonin (RETARD) provides a more appropriate option for contrasting these dysfunctions compared with rapid release melatonin (FAST) administration.

Indexed as

Oxidative StressAgingAnimalsAntioxidantsAtherosclerosisCells, CulturedDisease Models, AnimalEndothelium, VascularMaleMelatoninMiceMice, Inbred C57BLRadioimmunoassayUp-RegulationVasodilationAntioxidantsMelatonin

Identifiers

PMID22109832
PMCPMC3543744
OpenAlexW2067315679

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.