Evidence map›Paper›PMID 21712363›Full record

ReviewEndocrinology2011

Minireview: cracking the metabolic code for thyroid hormone signaling.

Antonio C Bianco

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. A study of the role of DIO1 and DIO2 polymorphism in thyroid cancer and drug response to therapy in the Saudi population.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2019
    Article
  10. Review
  11. Review
  12. Article
  13. Targeting iodothyronine deiodinases locally in the retina is a therapeutic strategy for retinal degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  14. Article
  15. A review of the peripheral levels of regulation by thyroid hormone.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016
    Review
  16. Article
  17. Article
  18. The brown fat secretome: metabolic functions beyond thermogenesis.Trends in endocrinology and metabolism: TEM · 2015
    Review
  19. Article
  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

1 author at 1 institution in 1 country.

Antonio C BiancoDivision of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, 1400 North West 10th Avenue, Suite 816, Miami, Florida 33136, USA. abianco@deiodinase.org
University of Miami · US

Funding

SELENODEIODINAS PROCESSING BY THE PROTEASOME SYSTEMR01DK058538 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIANCO, ANTONIO C, GEREBEN, BALÁZS · 2001 to 2024
$6.0M
Metabolic and Xenobiotic Control of Thyroid Hormone MetabolismR01DK077148 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ANTONIO C BIANCO · 2007 to 2026
$4.5M
Thyroid-adrenergic synergism and adaptive thermogenesisR01DK065055 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIANCO, ANTONIO C · 2005 to 2021
$4.4M
NIDDK NIH HHS DK58538NIDDK NIH HHS DK65055NIDDK NIH HHS DK77148NIDDK NIH HHS DK7856NIDDK NIH HHS R01 DK058538NIDDK NIH HHS R01 DK065055NIDDK NIH HHS R01 DK077148
6 · The paper itself

Abstract

Cells are not passive bystanders in the process of hormonal signaling and instead can actively customize hormonal action. Thyroid hormone gains access to the intracellular environment via membrane transporters, and while diffusing from the plasma membrane to the nucleus, thyroid hormone signaling is modified via the action of the deiodinases. Although the type 2 deiodinase (D2) converts the prohormone T(4) to the biologically active T(3), the type 3 deiodinase (D3) converts it to reverse T(3), an inactive metabolite. D3 also inactivates T(3) to T(2), terminating thyroid hormone action. Therefore, D2 confers cells with the capacity to produce extra amounts of T(3) and thus enhances thyroid hormone signaling. In contrast expression of D3 results in the opposite action. The Dio2 and Dio3 genes undergo transcriptional regulation throughout embryonic development, childhood, and adult life. In addition, the D2 protein is unique in that it can be switched off and on via an ubiquitin regulated mechanism, triggered by catalysis of T(4). Induction of D2 enhances local thyroid hormone signaling and energy expenditure during activation of brown adipose tissue by cold exposure or high-fat diet. On the other hand, induction of D3 in myocardium and brain during ischemia and hypoxia decreases energy expenditure as part of a homeostatic mechanism to slow down cell metabolism in the face of limited O(2) supply.

Indexed as

AnimalsBone and BonesHumansHypothalamusIodide PeroxidaseSignal TransductionThyroid HormonesIodide PeroxidaseThyroid Hormones

Identifiers

PMID21712363
PMCPMC3159779
OpenAlexW2048983470

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.