Evidence map›Paper›PMID 24713655›Full record

ArticleThe Journal of clinical investigation2014

Autophagy-regulating TP53INP2 mediates muscle wasting and is repressed in diabetes.

David Sala, Saška Ivanova, Natàlia Plana, Vicent Ribas, Jordi Duran, Daniel Bach, Saadet Turkseven, Martine Laville, Hubert Vidal, Monika Karczewska-Kupczewska and 7 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 4 pooled it
5.6field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 4 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Guideline
  4. Pooled it
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. The proteasome regulates body weight and systemic nutrient metabolism during fasting.American journal of physiology. Endocrinology and metabolism · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Cells · 2021
    Article
  18. Review
  19. Article
  20. 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

17 authors at 9 institutions in 4 countries.

David Sala
Saška Ivanova
Natàlia Plana
Vicent Ribas
Jordi Duran
Daniel Bach
Saadet Turkseven
Martine Laville
Hubert Vidal
Monika Karczewska-Kupczewska
Irina Kowalska
Marek Straczkowski
Xavier Testar
Manuel Palacín
Marco Sandri
Antonio L Serrano
Antonio Zorzano
Institute for Research in Biomedicine · ESInstituto de Salud Carlos III · ESLaboratoire CarMeN · FRUniversitat de Barcelona · ESInstitute of Animal Reproduction and Food Research · PLInstituto de Investigación de Enfermedades Raras · ESPolish Academy of Sciences · PLUniversitat Pompeu Fabra · ESVeneto Institute of Molecular Medicine · IT

Funding

Telethon TCR09003
6 · The paper itself

Abstract

A precise balance between protein degradation and synthesis is essential to preserve skeletal muscle mass. Here, we found that TP53INP2, a homolog of the Drosophila melanogaster DOR protein that regulates autophagy in cellular models, has a direct impact on skeletal muscle mass in vivo. Using different transgenic mouse models, we demonstrated that muscle-specific overexpression of Tp53inp2 reduced muscle mass, while deletion of Tp53inp2 resulted in muscle hypertrophy. TP53INP2 activated basal autophagy in skeletal muscle and sustained p62-independent autophagic degradation of ubiquitinated proteins. Animals with muscle-specific overexpression of Tp53inp2 exhibited enhanced muscle wasting in streptozotocin-induced diabetes that was dependent on autophagy; however, TP53INP2 ablation mitigated experimental diabetes-associated muscle loss. The overexpression or absence of TP53INP2 did not affect muscle wasting in response to denervation, a condition in which autophagy is blocked, further indicating that TP53INP2 alters muscle mass by activating autophagy. Moreover, TP53INP2 expression was markedly repressed in muscle from patients with type 2 diabetes and in murine models of diabetes. Our results indicate that TP53INP2 negatively regulates skeletal muscle mass through activation of autophagy. Furthermore, we propose that TP53INP2 repression is part of an adaptive mechanism aimed at preserving muscle mass under conditions in which insulin action is deficient.

Indexed as

AutophagyGene Expression RegulationAnimalsDiabetes ComplicationsDiabetes Mellitus, ExperimentalDrosophila melanogasterMice, KnockoutMuscular AtrophyNuclear ProteinsNuclear Proteins

Identifiers

PMID24713655
PMCPMC4001546
OpenAlexW2064790354

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.