Evidence map›Paper›PMID 37740833›Full record

ReviewEndocrine2024

Gene polymorphisms and thyroid hormone signaling: implication for the treatment of hypothyroidism.

Gustavo C Penna, Federico Salas-Lucia, Miriam O Ribeiro, Antonio C Bianco

Open access · greenAbstract readReview
In one paragraph

Review in Endocrine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. 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

4 authors at 2 institutions in 2 countries.

Gustavo C PennaSection of Adult and Pediatric Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, IL, USA.
Federico Salas-LuciaSection of Adult and Pediatric Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, IL, USA.
Miriam O RibeiroDevelopmental Disorders Program, Center for Biological Sciences and Health, Mackenzie Presbyterian University, Sao Paulo, SP, Brazil.
Antonio C BiancoSection of Adult and Pediatric Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, IL, USA. abianco1@uchicago.edu.ORCID 0000-0001-7737-6813
University of Chicago · USUniversidade Presbiteriana Mackenzie · BR

Funding

THYROID PHYSIOLOGY STUDIES OF INHERITED DISORDERSR01DK015070 · NIDDK · UNIVERSITY OF CHICAGO · PI ANTONIO C BIANCO, Alexandra Mihaela Dumitrescu · 1986 to 2026
$8.1M
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 PHYSIOLOGY STUDIES OF INHERITED DISORDERSR37DK015070 · NIDDK · UNIVERSITY OF CHICAGO · PI REFETOFF, SAMUEL · 1989 to 2015
$5.6M
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
Atrial natriuretic peptide receptor crystallizationR21DK065066 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI VAN DEN AKKER, FOCCO · 2003 to 2004
$306k
Selenodeidinase Processing by the Proteasome SystemR56DK058538 · NIDDK · UNIVERSITY OF CHICAGO · PI BIANCO, ANTONIO C · 2019 to 2019
$203k
NIDDK NIH HHS R01 DK015070NIDDK NIH HHS R01 DK058538NIDDK NIH HHS R01 DK065055NIDDK NIH HHS R01 DK077148NIDDK NIH HHS R21 DK065066NIDDK NIH HHS R37 DK015070NIDDK NIH HHS R56 DK058538
6 · The paper itself

Abstract

introductionMutations and single nucleotide polymorphisms (SNPs) in the genes encoding the network of proteins involved in thyroid hormone signaling (TH) may have implications for the effectiveness of the treatment of hypothyroidism with LT4. It is conceivable that loss-of-function mutations or SNPs impair the ability of LT4 to be activated to T3, reach its targets, and ultimately resolve symptoms of hypothyroidism. Some of these patients do benefit from therapy containing LT4 and LT3.

methodsHere, we reviewed the PubMed and examined gene mutations and SNPs in the TH cellular transporters, deiodinases, and TH receptors, along with their impact on TH signaling, and potential clinical implications.

resultsIn some mechanisms, such as the Thr92Ala-DIO2 SNP, there is a compelling rationale for reduced T4 to T3 activation that limits the effectiveness of LT4 to restore euthyroidism. In other mechanisms, a potential case can be made but more studies with a larger number of individuals are needed. DISCUSSION/

conclusionUnderstanding the clinical impact of the genetic makeup of LT4-treated patients may help in the preemptive identification of those individuals that would benefit from therapy containing LT3.

Indexed as

HypothyroidismPolymorphism, Single NucleotideSignal TransductionThyroid HormonesHumansThyroid HormonesdeiodinasepolymorphismT3-signalingthyroidthyroxinetriiodothyronine

Identifiers

PMID37740833
PMCPMC10959761
OpenAlexW4386981191

What Socratic holds

Textmetadata
LicenceTDM
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.