Evidence map›Paper›PMID 26953569›Full record

ArticlePloS one2016

Tissue-Specific Suppression of Thyroid Hormone Signaling in Various Mouse Models of Aging.

W Edward Visser, Cíntia R Bombardieri, Chantal Zevenbergen, Sander Barnhoorn, Alexandre Ottaviani, Ingrid van der Pluijm, Renata Brandt, Ellen Kaptein, Ramona van Heerebeek, Hans van Toor and 17 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Thyroid dysfunction in ageing populations.Endocrine connections · 2025
    Review
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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

27 authors at 9 institutions in 4 countries.

W Edward VisserDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Cíntia R BombardieriMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Chantal ZevenbergenDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Sander BarnhoornMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Alexandre OttavianiMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Ingrid van der PluijmMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Renata BrandtMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Ellen KapteinDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Ramona van HeerebeekDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Hans van ToorDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
George A GarinisMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Robin P PeetersDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Marco MediciDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Willy van HamLaboratory of Comparative Endocrinology, Biology Department, KULeuven, Leuven, Belgium.
Wilbert P VermeijMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Monique C de WaardMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Ronald R de KrijgerDept of Pathology, Erasmus Medical Center, Rotterdam, The Netherlands.
Anita BoelenDept of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands.
Joan KwakkelDept of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands.
John J KopchickDept of Biomedical Sciences, Edison Biotechnology Institute, Ohio University, Athens, Ohio, United States of America.
Edward O ListDept of Biomedical Sciences, Edison Biotechnology Institute, Ohio University, Athens, Ohio, United States of America.
Joost P M MelisDept of Toxicogenetics, Leiden University Medical Center, Leiden, The Netherlands.
Veerle M DarrasLaboratory of Comparative Endocrinology, Biology Department, KULeuven, Leuven, Belgium.
Martijn E T DolléCentre for Health Protection Research, National Institute of Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Gijsbertus T J van der HorstMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Jan H J HoeijmakersMGC Dept of Genetics, Cancer Genomics Center, Erasmus Medical Center, Rotterdam, The Netherlands.
Theo J VisserDept of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Cancer Genomics Centre · NLErasmus MC · NLAcademic Medical Center · NLKU Leuven · BEBiotechnology Institute · USCentre National de la Recherche Scientifique · FRLeiden University Medical Center · NLNational Institute for Public Health and the Environment · NLOhio University · US

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
Models for DNA repair and cell cycle control variantsU01ES011044 · NIEHS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 2001 to 2006
$5.1M
NIA NIH HHS 1P01 AG-17242-02NIA NIH HHS P01 AG017242NIEHS NIH HHS 1UO1 ES011044NIEHS NIH HHS U01 ES011044
6 · The paper itself

Abstract

DNA damage contributes to the process of aging, as underscored by premature aging syndromes caused by defective DNA repair. Thyroid state changes during aging, but underlying mechanisms remain elusive. Since thyroid hormone (TH) is a key regulator of metabolism, changes in TH signaling have widespread effects. Here, we reveal a significant common transcriptomic signature in livers from hypothyroid mice, DNA repair-deficient mice with severe (Csbm/m/Xpa-/-) or intermediate (Ercc1-/Δ-7) progeria and naturally aged mice. A strong induction of TH-inactivating deiodinase D3 and decrease of TH-activating D1 activities are observed in Csbm/m/Xpa-/- livers. Similar findings are noticed in Ercc1-/Δ-7, in naturally aged animals and in wild-type mice exposed to a chronic subtoxic dose of DNA-damaging agents. In contrast, TH signaling in muscle, heart and brain appears unaltered. These data show a strong suppression of TH signaling in specific peripheral organs in premature and normal aging, probably lowering metabolism, while other tissues appear to preserve metabolism. D3-mediated TH inactivation is unexpected, given its expression mainly in fetal tissues. Our studies highlight the importance of DNA damage as the underlying mechanism of changes in thyroid state. Tissue-specific regulation of deiodinase activities, ensuring diminished TH signaling, may contribute importantly to the protective metabolic response in aging.

Indexed as

DNA DamageAgingAnimalsHypothyroidismIodide PeroxidaseLiverMiceMice, KnockoutOrgan SpecificityThyroid HormonesIodide PeroxidaseThyroid Hormones

Identifiers

PMID26953569
PMCPMC4783069
OpenAlexW2294573042

What OpenQuestion holds

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LicenceCC BY
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.