Evidence map›Paper›PMID 31941062›Full record

ReviewCells2020

Mitochondrial Mechanisms of Neuromuscular Junction Degeneration with Aging.

Maria-Eleni Anagnostou, Russell T Hepple

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Circulating Mediators of Apoptosis and Inflammation in Aging; Physical Exercise Intervention.International journal of environmental research and public health · 2021
    Trial
  3. Article
  4. Review
  5. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Motor performance and aging in males and females.Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. The link between Mitochondria and Sarcopenia.Journal of physiology and biochemistry · 2025
    Review
  20. Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Maria-Eleni AnagnostouDepartment of Physical Therapy and Department of Physiology & Functional Genomics, University of Florida, Gainesville, FL 32608, USA.
Russell T HeppleDepartment of Physical Therapy and Department of Physiology & Functional Genomics, University of Florida, Gainesville, FL 32608, USA.ORCID 0000-0003-3640-486X
University of Florida · US

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI CHRISTIAAN LEEUWENBURGH · 2007 to 2026
$22.8M
CIHRNIA NIH HHS P30 AG028740
6 · The paper itself

Abstract

Skeletal muscle deteriorates with aging, contributing to physical frailty, poor health outcomes, and increased risk of mortality. Denervation is a major driver of changes in aging muscle. This occurs through transient denervation-reinnervation events throughout the aging process that remodel the spatial domain of motor units and alter fiber type. In advanced age, reinnervation wanes, leading to persistent denervation that accelerates muscle atrophy and impaired muscle contractility. Alterations in the muscle fibers and motoneurons are both likely involved in driving denervation through destabilization of the neuromuscular junction. In this respect, mitochondria are implicated in aging and age-related neurodegenerative disorders, and are also likely key to aging muscle changes through their direct effects in muscle fibers and through secondary effects mediated by mitochondrial impairments in motoneurons. Indeed, the large abundance of mitochondria in muscle fibers and motoneurons, that are further concentrated on both sides of the neuromuscular junction, likely renders the neuromuscular junction especially vulnerable to age-related mitochondrial dysfunction. Manifestations of mitochondrial dysfunction with aging include impaired respiratory function, elevated reactive oxygen species production, and increased susceptibility to permeability transition, contributing to reduced ATP generating capacity, oxidative damage, and apoptotic signaling, respectively. Using this framework, in this review we summarize our current knowledge, and relevant gaps, concerning the potential impact of mitochondrial impairment on the aging neuromuscular junction, and the mechanisms involved.

Indexed as

AgingAnimalsHumansMitochondriaMuscle, SkeletalNeuromuscular Junctionagingmitochondriamotoneuronmuscle atrophyneuromuscular junctionskeletal muscle

Identifiers

PMID31941062
PMCPMC7016881
OpenAlexW2999368944

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.