Evidence map›Paper›PMID 35765148›Full record

ArticleJournal of cachexia, sarcopenia and muscle2022

Combined fibre atrophy and decreased muscle regeneration capacity driven by mitochondrial DNA alterations underlie the development of sarcopenia.

Sammy Kimoloi, Ayesha Sen, Stefan Guenther, Thomas Braun, Tobias Brügmann, Philipp Sasse, Rudolf J Wiesner, David Pla-Martín, Olivier R Baris

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  9. Innately expressed estrogen-related receptors in the skeletal muscle are indispensable for exercise fitness.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  10. Review
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  12. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    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

9 authors at 4 institutions in 4 countries.

Sammy KimoloiInstitute of Vegetative Physiology, University of Cologne, Faculty of Medicine and University Clinics, Köln, Germany.
Ayesha SenInstitute of Vegetative Physiology, University of Cologne, Faculty of Medicine and University Clinics, Köln, Germany.
Stefan GuentherMax Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Thomas BraunMax Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Tobias BrügmannInstitute for Cardiovascular Physiology, University Medical Center, Göttingen, Germany.
Philipp SasseInstitute of Physiology I, Medical Faculty, University of Bonn, Bonn, Germany.
Rudolf J WiesnerInstitute of Vegetative Physiology, University of Cologne, Faculty of Medicine and University Clinics, Köln, Germany.ORCID 0000-0003-1677-4476
David Pla-MartínInstitute of Vegetative Physiology, University of Cologne, Faculty of Medicine and University Clinics, Köln, Germany.ORCID 0000-0002-5189-0723
Olivier R BarisInstitute of Vegetative Physiology, University of Cologne, Faculty of Medicine and University Clinics, Köln, Germany.ORCID 0000-0003-0974-6856
University of Cologne · DEMax Planck Institute for Heart and Lung Research · DEUniversity of Bonn · DECentre National de la Recherche Scientifique · FR

Funding

Agence Nationale de la Recherche/Deutsche Forschungsgemeinschaft ANR-20-CE92-0020Deutsche Forschungsgemeinschaft PL895/1-1Deutsche Forschungsgemeinschaft SFB 1218/TP B07Deutscher Akademischer Austauschdienst 91524219Köln Fortune, Faculty of Medicine. University of Cologne 34/2019
6 · The paper itself

Abstract

backgroundMitochondrial dysfunction caused by mitochondrial (mtDNA) deletions have been associated with skeletal muscle atrophy and myofibre loss. However, whether such defects occurring in myofibres cause sarcopenia is unclear. Also, the contribution of mtDNA alterations in muscle stem cells (MuSCs) to sarcopenia remains to be investigated.

methodsWe expressed a dominant-negative variant of the mitochondrial helicase, which induces mtDNA alterations, specifically in differentiated myofibres (K320E

resultsK320E

conclusionsTaken together, accumulation of large-scale mtDNA alterations in myofibres alone is not sufficient to cause sarcopenia. Expression of K320E-Twinkle is tolerated in quiescent MuSCs, but progressively leads to mtDNA and respiratory chain depletion upon activation, in vivo and in vitro, possibly caused by an increased mitochondrial removal. Altogether, our results suggest that the accumulation of mtDNA alterations in myofibres activates regeneration during aging, which leads to sarcopenia if such alterations have expanded in MuSCs as well.

Indexed as

SarcopeniaAnimalsDNA, MitochondrialMiceMitochondriaMuscle, SkeletalRegenerationDNA, MitochondrialMitochondriamtDNA deletionsMuscle stem cellsMutationsMyofibresSatellite cells

Identifiers

PMID35765148
PMCPMC9397496
OpenAlexW4283689274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.