Evidence map›Paper›PMID 27561813›Full record

ArticleAging cell2016

Latent mitochondrial DNA deletion mutations drive muscle fiber loss at old age.

Allen Herbst, Jonathan Wanagat, Nashwa Cheema, Kevin Widjaja, Debbie McKenzie, Judd M Aiken

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.9field-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

44 citing papers in PubMed, 76 citations in OpenAlex.

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  12. Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023
    Review
  13. Article
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  15. Review
  16. Stochastic survival of the densest and mitochondrial DNA clonal expansion in aging.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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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 3 institutions in 2 countries.

Allen HerbstCentre for Prions and Protein Folding Diseases, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, AB, Canada.
Jonathan WanagatDivision of Geriatrics, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Nashwa CheemaCentre for Prions and Protein Folding Diseases, Department of Biological Sciences, University of Alberta, Edmonton, AB, Canada.
Kevin WidjajaDivision of Geriatrics, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Debbie McKenzieCentre for Prions and Protein Folding Diseases, Department of Biological Sciences, University of Alberta, Edmonton, AB, Canada.
Judd M AikenCentre for Prions and Protein Folding Diseases, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, AB, Canada.
University of Alberta · CAUniversity of California, Los Angeles · USUniversity of California System · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
UCLA OLDER AMERICANS INDEPENDENCE CENTERP30AG028748 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REUBEN, DAVID B. · 2006 to 2017
$9.8M
Impact of Exercise on SarcopeniaR01AG030423 · NIA · UNIVERSITY OF ALBERTA · PI AIKEN, JUDD M. · 2009 to 2013
$2.1M
Mitochondrial genetics in skeletal muscle agingK08AG032873 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANAGAT, JONATHAN · 2009 to 2013
$473k
American Federation for Aging ResearchCanada Foundation for Innovation LOF24776Ellison Medical Foundation New Scholar AwardGlenn Foundation for Medical ResearchNIA NIH HHS K08 AG032873NIA NIH HHS P30 AG028748NIA NIH HHS R01 AG030423NIDDK NIH HHS P30 DK063491NIH-NCRR CJX1-443835-WS-29646NSF Major Research Instrumentation CHE-0722519Senior Scholar AwardUCLA Hartford Center of ExcellenceUCSD/UCLA Diabetes Research Center Pilot and Feasibility Grant
6 · The paper itself

Abstract

With age, somatically derived mitochondrial DNA (mtDNA) deletion mutations arise in many tissues and species. In skeletal muscle, deletion mutations clonally accumulate along the length of individual fibers. At high intrafiber abundances, these mutations disrupt individual cell respiration and are linked to the activation of apoptosis, intrafiber atrophy, breakage, and necrosis, contributing to fiber loss. This sequence of molecular and cellular events suggests a putative mechanism for the permanent loss of muscle fibers with age. To test whether mtDNA deletion mutation accumulation is a significant contributor to the fiber loss observed in aging muscle, we pharmacologically induced deletion mutation accumulation. We observed a 1200% increase in mtDNA deletion mutation-containing electron transport chain-deficient muscle fibers, an 18% decrease in muscle fiber number and 22% worsening of muscle mass loss. These data affirm the hypothesized role for mtDNA deletion mutation in the etiology of muscle fiber loss at old age.

Indexed as

agingmitochondrial DNA deletion mutationmusclesarcopenia

Identifiers

PMID27561813
PMCPMC5114866
OpenAlexW2507891142

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.