Evidence map›Paper›PMID 34822388›Full record

ReviewMetabolites2021

Thyroid Hormone Action in Muscle Atrophy.

Maria Angela De Stefano, Raffaele Ambrosio, Tommaso Porcelli, Gianfranco Orlandino, Domenico Salvatore, Cristina Luongo

Open access · goldAbstract readReview
In one paragraph

Review in Metabolites, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2026
    Article
  5. Article
  6. Thyrotoxicosis in MCT8 deficiency.The Journal of clinical endocrinology and metabolism · 2026
    Review
  7. Article
  8. Chronic thyrotoxic myopathy in an 81-year-old man with Graves disease.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Deiodinases in thyroid tumorigenesis.Endocrine-related cancer · 2023
    Review
  18. Article
  19. Article
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

6 authors at 3 institutions in 1 country.

Maria Angela De StefanoDepartment of Clinical Medicine and Surgery, University of Naples Federico II, 80131 Naples, Italy.
Raffaele AmbrosioIstituti di Ricovero e Cura a Carattere Scientifico, SDN, 80143 Naples, Italy.
Tommaso PorcelliDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.
Gianfranco OrlandinoAzienda Ospedaliera Universitaria Federico II, 80131 Naples, Italy.
Domenico SalvatoreDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0002-4556-7620
Cristina LuongoDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.
University of Naples Federico II · ITFederico II University Hospital · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle atrophy is a condition associated with various physiological and pathophysiological conditions, such as denervation, cachexia, and fasting. It is characterized by an altered protein turnover in which the rate of protein degradation exceeds the rate of protein synthesis, leading to substantial muscle mass loss and weakness. Muscle protein breakdown reflects the activation of multiple proteolytic mechanisms, including lysosomal degradation, apoptosis, and ubiquitin-proteasome. Thyroid hormone (TH) plays a key role in these conditions. Indeed, skeletal muscle is among the principal TH target tissue, where TH regulates proliferation, metabolism, differentiation, homeostasis, and growth. In physiological conditions, TH stimulates both protein synthesis and degradation, and an alteration in TH levels is often responsible for a specific myopathy. Intracellular TH concentrations are modulated in skeletal muscle by a family of enzymes named deiodinases; in particular, in muscle, deiodinases type 2 (D2) and type 3 (D3) are both present. D2 activates the prohormone T4 into the active form triiodothyronine (T3), whereas D3 inactivates both T4 and T3 by the removal of an inner ring iodine. Here we will review the present knowledge of TH action in skeletal muscle atrophy, in particular, on the molecular mechanisms presiding over the control of intracellular T3 concentration in wasting muscle conditions. Finally, we will discuss the possibility of exploiting the modulation of deiodinases as a possible therapeutic approach to treat muscle atrophy.

Indexed as

deiodinasemuscle atrophythyroid hormone

Identifiers

PMID34822388
PMCPMC8625289
OpenAlexW3211021622

What OpenQuestion holds

Textmetadata
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.