Evidence map›Paper›PMID 33720335›Full record

ReviewEndocrinology2021

Deiodinases and the Metabolic Code for Thyroid Hormone Action.

Samuel C Russo, Federico Salas-Lucia, Antonio C Bianco

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.6field-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

59 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Endocrine-Metabolic Crosstalk Between Diabetes Mellitus and Hypothyroidism: From Network Mechanisms to Translational Stratification.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Review
  4. Article
  5. Cardiometabolic Risk Factors in Women Exposed to High Altitude.International journal of molecular sciences · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Critical Role of Iodine and Thyroid Hormones During Pregnancy.International journal of molecular sciences · 2025
    Review
  19. 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

3 authors at 1 institution in 1 country.

Samuel C RussoSection of Endocrinology, Diabetes & Metabolism, University of Chicago Medical Center, Chicago, IL 60637, USA.
Federico Salas-LuciaSection of Endocrinology, Diabetes & Metabolism, University of Chicago Medical Center, Chicago, IL 60637, USA.
Antonio C BiancoSection of Endocrinology, Diabetes & Metabolism, University of Chicago Medical Center, Chicago, IL 60637, USA.ORCID 0000-0001-7737-6813
University of Chicago Medical Center · 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
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 R01 DK058538NIDDK NIH HHS R01 DK065055
6 · The paper itself

Abstract

Deiodinases modify the biological activity of thyroid hormone (TH) molecules, ie, they may activate thyroxine (T4) to 3,5,3'-triiodothyronine (T3), or they may inactivate T3 to 3,3'-diiodo-L-thyronine (T2) or T4 to reverse triiodothyronine (rT3). Although evidence of deiodination of T4 to T3 has been available since the 1950s, objective evidence of TH metabolism was not established until the 1970s. The modern paradigm considers that the deiodinases not only play a role in the homeostasis of circulating T3, but they also provide dynamic control of TH signaling: cells that express the activating type 2 deiodinase (D2) have enhanced TH signaling due to intracellular build-up of T3; the opposite is seen in cells that express type 3 deiodinase (D3), the inactivating deiodinase. D2 and D3 are expressed in metabolically relevant tissues such as brown adipose tissue, skeletal muscle and liver, and their roles have been investigated using cell, animal, and human models. During development, D2 and D3 expression customize for each tissue/organ the timing and intensity of TH signaling. In adult cells, D2 is induced by cyclic adenosine monophosphate (cAMP), and its expression is invariably associated with enhanced T3 signaling, expression of PGC1 and accelerated energy expenditure. In contrast, D3 expression is induced by hypoxia-inducible factor 1α (HIF-1a), dampening T3 signaling and the metabolic rate. The coordinated expression of these enzymes adjusts TH signaling in a time- and tissue-specific fashion, affecting metabolic pathways in health and disease states.

Indexed as

Adipose Tissue, BrownAnimalsFastingHumansIodide PeroxidaseIodothyronine Deiodinase Type IIThyroid HormonesIodide PeroxidaseIodothyronine Deiodinase Type IIiodothyronine deiodinase type IIIThyroid Hormonesdeiodinaseenergy expendituremetabolic rateoxygen consumptionthermogenesisthyroidthyroxinetriiodothyronine

Identifiers

PMID33720335
PMCPMC8237994
OpenAlexW3135995479

What Socratic 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 Socratic graph.