Evidence map›Paper›PMID 32905522›Full record

ArticleJCSM rapid communications

The wasting-associated metabolite succinate disrupts myogenesis and impairs skeletal muscle regeneration.

Paige C Arneson-Wissink, Kelly A Hogan, Alexandra M Ducharme, Adrienne Samani, Aminah Jatoi, Jason D Doles

Open access · goldAbstract read
In one paragraph

Article in JCSM rapid communications. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Macrophage immunometabolism: emerging targets for regrowth in aging muscle.American journal of physiology. Endocrinology and metabolism · 2025
    Review
  4. Article
  5. Review
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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

6 authors at 1 institution in 1 country.

Paige C Arneson-WissinkDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, 55905 USA.
Kelly A HoganDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, 55905 USA.
Alexandra M DucharmeDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, 55905 USA.
Adrienne SamaniDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, 55905 USA.
Aminah JatoiDepartment of Oncology, Mayo Clinic, Rochester, Minnesota.
Jason D DolesDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, 55905 USA.
Mayo Clinic · US

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D, PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
Mechanisms of sepsis-associated muscle stem cell dysfunctionR35GM128594 · NIGMS · MAYO CLINIC ROCHESTER · PI DOLES, JASON · 2018 to 2022
$2.0M
Role of Vav1 protooncogene in pancreatic cancerP20CA102701 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI PETERSEN, GLORIA M. · 2003 to 2003
$1.5M
Post-transcriptional Regulation of Satellite Cell FunctionR00AR066696 · NIAMS · MAYO CLINIC ROCHESTER · PI DOLES, JASON · 2016 to 2018
$961k
Post-transcriptional Regulation of Satellite Cell FunctionK99AR066696 · NIAMS · UNIVERSITY OF COLORADO · PI DOLES, JASON · 2015 to 2015
$93k
NCI NIH HHS P20 CA102701NCI NIH HHS P50 CA102701NIAMS NIH HHS K99 AR066696NIAMS NIH HHS R00 AR066696NIGMS NIH HHS R35 GM128594
6 · The paper itself

Abstract

Background: Muscle wasting is a debilitating co-morbidity affecting most advanced cancer patients. Alongside enhanced muscle catabolism, defects in muscle repair/regeneration contribute to cancer-associated wasting. Among the factors implicated in suppression of muscle regeneration are cytokines that interfere with myogenic signal transduction pathways. Less understood is how other cancer/wasting-associated cues, such as metabolites, contribute to muscle dysfunction. This study investigates how the metabolite succinate affects myogenesis and muscle regeneration. Methods: We leveraged an established ectopic metabolite treatment (cell permeable dimethyl-succinate) strategy to evaluate the ability of intracellular succinate elevation to 1) affect myoblast homeostasis (proliferation, apoptosis), 2) disrupt protein dynamics and induce wasting-associated atrophy, and 3) modulate Results: We found that Conclusions: This study broadens the repertoire of wasting-associated factors that can directly modulate muscle progenitor cell function and strengthens the hypothesis that metabolic derangements are significant contributors to impaired muscle regeneration, an important aspect of cancer-associated muscle wasting.

Indexed as

Muscle wastingmyogenesisskeletal musclesuccinate

Identifiers

PMID32905522
PMCPMC7470228
OpenAlexW3033924432

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.