Evidence map›Paper›PMID 35406681›Full record

ArticleCells2022

Activin A Causes Muscle Atrophy through MEF2C-Dependent Impaired Myogenesis.

Audrey Loumaye, Pascale Lause, Xiaoling Zhong, Teresa A Zimmers, Laure B Bindels, Jean-Paul Thissen

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  9. Article
  10. The Role of theAnimals : an open access journal from MDPI · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  15. Article
  16. 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

6 authors at 3 institutions in 2 countries.

Audrey LoumayePole of Endocrinology, Diabetology and Nutrition, Institute of Experimental and Clinical Research, Université Catholique de Louvain, 1200 Brussels, Belgium.ORCID 0000-0003-2887-0721
Pascale LausePole of Endocrinology, Diabetology and Nutrition, Institute of Experimental and Clinical Research, Université Catholique de Louvain, 1200 Brussels, Belgium.
Xiaoling ZhongDepartment of Surgery, Indiana University School of Medicine, Indiana University Simon and Bren Comprehensive Cancer Center, Richard L. Roudebush Veterans Administration Medical Center, Indianapolis, IN 46202, USA.
Teresa A ZimmersDepartment of Surgery, Indiana University School of Medicine, Indiana University Simon and Bren Comprehensive Cancer Center, Richard L. Roudebush Veterans Administration Medical Center, Indianapolis, IN 46202, USA.ORCID 0000-0001-7872-0540
Laure B BindelsMetabolism and Nutrition Research Group, Louvain Drug Research Institute, Université Catholique de Louvain, 1200 Brussels, Belgium.ORCID 0000-0003-3747-3234
Jean-Paul ThissenPole of Endocrinology, Diabetology and Nutrition, Institute of Experimental and Clinical Research, Université Catholique de Louvain, 1200 Brussels, Belgium.
Cliniques Universitaires Saint-Luc · BERichard L. Roudebush VA Medical Center · USUCLouvain · BE

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Jun Wan · 1999 to 2026
$59.3M
The role of the macroenvironment in pancreatic cancer-induced cachexiaP01CA236778 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI GUTTRIDGE, DENIS C · 2021 to 2025
$9.7M
Molecular Mechanisms of Muscle and Fat Wasting in Pancreatic Cancer CachexiaI01BX004177 · VA · RLR VA MEDICAL CENTER · PI ZIMMERS, TERESA A · 2018 to 2021
–
Tumor tissue crosstalk in the macroenvironment of pancreatic cancer cachexiaI01CX002046 · VA · RLR VA MEDICAL CENTER · PI ZIMMERS, TERESA A · 2020 to 2024
–
BLRD VA I01 BX004177CSRD VA I01 CX002046NCI NIH HHS P01 CA236778NCI NIH HHS P30 CA082709
6 · The paper itself

Abstract

Activin A (ActA) is considered to play a major role in cancer-induced cachexia (CC). Indeed, circulating ActA levels are elevated and predict survival in patients with CC. However, the mechanisms by which ActA mediates CC development and in particular skeletal muscle (SM) atrophy in humans are not yet fully understood. In this work, we aimed to investigate the effects of ActA on human SM and in mouse models of CC. We used a model of human muscle cells in culture to explore how ActA acts towards human SM. In this model, recombinant ActA induced myotube atrophy associated with the decline of MyHC-β/slow, the main myosin isoform in human muscle cells studied. Moreover, ActA inhibited the expression and activity of MEF2C, the transcription factor regulating

Indexed as

ActivinsMEF2 Transcription FactorsMuscular AtrophyMuscular DiseasesAnimalsCachexiaHumansMiceMuscle Developmentactivin AActivinsMEF2C protein, humanMef2c protein, mouseMEF2 Transcription Factorsactivin AMEF2Cmuscle atrophymyogenesisskeletal muscle

Identifiers

PMID35406681
PMCPMC8997966
OpenAlexW4220739111

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.