Evidence map›Paper›PMID 24322650›Full record

ReviewNature reviews. Endocrinology2014

Thyroid hormones and skeletal muscle--new insights and potential implications.

Domenico Salvatore, Warner S Simonides, Monica Dentice, Ann Marie Zavacki, P Reed Larsen

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 4 pooled it
6.9field-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

206 citing papers in PubMed, 4 syntheses or guidelines pooled it, 372 citations in OpenAlex.

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  20. Global loss of selenocysteine lyase in mice drives lipid accumulation in brown adipocytes.American journal of physiology. Endocrinology and metabolism · 2026
    Article

146 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 3 countries.

Domenico SalvatoreDepartment of Clinical Medicine and Surgery, University of Naples 'Federico II', Building 1, 1st floor, Via Pansini 5, 80131 Naples, Italy.
Warner S SimonidesLaboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Centre, van der Boechorststraat 7, 1081 BT, Amsterdam, Netherlands.
Monica DenticeDepartment of Clinical Medicine and Surgery, University of Naples 'Federico II', Building 1, 1st floor, Via Pansini 5, 80131 Naples, Italy.
Ann Marie ZavackiThyroid Section, Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, HIM room 641, Boston, MA 02115, USA.
P Reed LarsenThyroid Section, Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, HIM room 641, Boston, MA 02115, USA.
Brigham and Women's Hospital · USFederico II University Hospital · ITAmsterdam UMC Location Vrije Universiteit Amsterdam · NL

Funding

PHYSIOLOGY OF THYROID HORMONE-DEPENDENT GENE EXPRESSIONR01DK044128 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI LARSEN, PHILIP REED, ZAVACKI, ANN M · 1992 to 2018
$6.8M
NIDDK NIH HHS DK044128NIDDK NIH HHS R01 DK044128Telethon GGP11185
6 · The paper itself

Abstract

Thyroid hormone signalling regulates crucial biological functions, including energy expenditure, thermogenesis, development and growth. The skeletal muscle is a major target of thyroid hormone signalling. The type 2 and 3 iodothyronine deiodinases (DIO2 and DIO3, respectively) have been identified in skeletal muscle. DIO2 expression is tightly regulated and catalyses outer-ring monodeiodination of the secreted prohormone tetraiodothyronine (T4) to generate the active hormone tri-iodothyronine (T3). T3 can remain in the myocyte to signal through nuclear receptors or exit the cell to mix with the extracellular pool. By contrast, DIO3 inactivates T3 through removal of an inner-ring iodine. Regulation of the expression and activity of deiodinases constitutes a cell-autonomous, pre-receptor mechanism for controlling the intracellular concentration of T3. This local control of T3 activity is crucial during the various phases of myogenesis. Here, we review the roles of T3 in skeletal muscle development and homeostasis, with a focus on the emerging local deiodinase-mediated control of T3 signalling. Moreover, we discuss these novel findings in the context of both muscle homeostasis and pathology, and examine how skeletal muscle deiodinase activity might be therapeutically harnessed to improve satellite-cell-mediated muscle repair in patients with skeletal muscle disorders, muscle atrophy or injury.

Indexed as

AnimalsEnergy MetabolismGene ExpressionHumansMuscle, SkeletalMuscular DiseasesSignal TransductionThyroid HormonesTriiodothyronineThyroid HormonesTriiodothyronine

Identifiers

PMID24322650
PMCPMC4037849
OpenAlexW1981948323

What OpenQuestion 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 OpenQuestion graph.