Evidence map›Paper›PMID 36899852›Full record

ReviewCells2023

The Role of Mitophagy in Skeletal Muscle Damage and Regeneration.

Eirini Chatzinikita, Maria Maridaki, Konstantinos Palikaras, Michael Koutsilieris, Anastassios Philippou

Open access · goldFull text readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

34 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Article
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  7. Article
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  10. Review
  11. Article
  12. Article
  13. Estrogen-Related Receptor Alpha Promotes Skeletal Muscle Regeneration and Mitigates Muscular Dystrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025
    Review
  19. A window into intracellular events in myositis through subcellular proteomics.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  20. Review
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

5 authors at 1 institution in 1 country.

Eirini ChatzinikitaDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 115 27 Athens, Greece.ORCID 0000-0001-8086-3444
Maria MaridakiFaculty of Physical Education and Sport Science, National and Kapodistrian University of Athens, 172 37 Athens, Greece.ORCID 0000-0003-3458-4633
Konstantinos PalikarasDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 115 27 Athens, Greece.ORCID 0000-0001-6992-5560
Michael KoutsilierisDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 115 27 Athens, Greece.
Anastassios PhilippouDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 115 27 Athens, Greece.ORCID 0000-0003-0047-3003
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are cellular organelles that play an essential role in generating the chemical energy needed for the biochemical reactions in cells. Mitochondrial biogenesis, i.e., de novo mitochondria formation, results in enhanced cellular respiration, metabolic processes, and ATP generation, while autophagic clearance of mitochondria (mitophagy) is required to remove damaged or useless mitochondria. The balance between the opposing processes of mitochondrial biogenesis and mitophagy is highly regulated and crucial for the maintenance of the number and function of mitochondria as well as for the cellular homeostasis and adaptations to metabolic demands and extracellular stimuli. In skeletal muscle, mitochondria are essential for maintaining energy homeostasis, and the mitochondrial network exhibits complex behaviors and undergoes dynamic remodeling in response to various conditions and pathologies characterized by changes in muscle cell structure and metabolism, such as exercise, muscle damage, and myopathies. In particular, the involvement of mitochondrial remodeling in mediating skeletal muscle regeneration following damage has received increased attention, as modifications in mitophagy-related signals arise from exercise, while variations in mitochondrial restructuring pathways can lead to partial regeneration and impaired muscle function. Muscle regeneration (through myogenesis) following exercise-induced damage is characterized by a highly regulated, rapid turnover of poor-functioning mitochondria, permitting the synthesis of better-functioning mitochondria to occur. Nevertheless, essential aspects of mitochondrial remodeling during muscle regeneration remain poorly understood and warrant further characterization. In this review, we focus on the critical role of mitophagy for proper muscle cell regeneration following damage, highlighting the molecular mechanisms of the mitophagy-associated mitochondrial dynamics and network reformation.

Indexed as

MitochondriaMitophagyAutophagyMitochondrial DynamicsMuscle, Skeletalexercisemitochondrial biogenesismitochondrial networkmitophagymuscle damagemyogenesisregeneration

Identifiers

PMID36899852
PMCPMC10000750
OpenAlexW4321789818

What Socratic holds

Textfull text, public
LicenceCC BY
measurements read3
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 Socratic graph.