Evidence map›Paper›PMID 26365892›Full record

ArticleAging cell2015

Apoptosis and necrosis mediate skeletal muscle fiber loss in age-induced mitochondrial enzymatic abnormalities.

Nashwa Cheema, Allen Herbst, Debbie McKenzie, Judd M Aiken

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  9. Effects of Bioconverted Guava Leaf (International journal of molecular sciences · 2025
    Article
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  14. Review
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  16. Article
  17. The emerging roles of necroptosis in skeletal muscle health and disease.Pflugers Archiv : European journal of physiology · 2024
    Review
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Nashwa CheemaDepartment of Biological Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada.
Allen HerbstDepartment of Agricultural, Food and Nutritional Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada.
Debbie McKenzieDepartment of Biological Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada.
Judd M AikenDepartment of Agricultural, Food and Nutritional Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada.
University of Alberta · CA

Funding

Impact of Exercise on SarcopeniaR01AG030423 · NIA · UNIVERSITY OF ALBERTA · PI AIKEN, JUDD M. · 2009 to 2013
$2.1M
NIA NIH HHS R01 AG030423
6 · The paper itself

Abstract

Sarcopenia, the age-induced loss of skeletal muscle mass and function, results from the contributions of both fiber atrophy and loss of myofibers. We have previously characterized sarcopenia in FBN rats, documenting age-dependent declines in muscle mass and fiber number along with increased fiber atrophy and fibrosis in vastus lateralis and rectus femoris muscles. Concomitant with these sarcopenic changes is an increased abundance of mitochondrial DNA deletion mutations and electron transport chain (ETC) abnormalities. In this study, we used immunohistological and histochemical approaches to define cell death pathways involved in sarcopenia. Activation of muscle cell death pathways was age-dependent with most apoptotic and necrotic muscle fibers exhibiting ETC abnormalities. Although activation of apoptosis was a prominent feature of electron transport abnormal muscle fibers, necrosis was predominant in atrophic and broken ETC-abnormal fibers. These data suggest that mitochondrial dysfunction is a major contributor to the activation of cell death processes in aged muscle fibers. The link between ETC abnormalities, apoptosis, fiber atrophy, and necrosis supports the hypothesis that mitochondrial DNA deletion mutations are causal in myofiber loss. These studies suggest a progression of events beginning with the generation and accumulation of a mtDNA deletion mutation, the concomitant development of ETC abnormalities, a subsequent triggering of apoptotic and, ultimately, necrotic events resulting in muscle fiber atrophy, breakage, and fiber loss.

Indexed as

AgingAnimalsApoptosisBiomarkersDNA, MitochondrialElectron TransportMaleMitochondriaMuscle Fibers, SkeletalNecrosisQuadriceps MuscleRatsRats, Inbred F344SarcopeniaSequence DeletionBiomarkersDNA, Mitochondrialagingapoptosiscell deathETS abnormalitiesmitochondrianecrosissarcopeniaskeletal muscle

Identifiers

PMID26365892
PMCPMC4693455
OpenAlexW1888940543

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.