Evidence map›Paper›PMID 36604839›Full record

ArticleJournal of cachexia, sarcopenia and muscle2023

Mitochondria transplant therapy improves regeneration and restoration of injured skeletal muscle.

Stephen E Alway, Hector G Paez, Christopher R Pitzer, Peter J Ferrandi, Mohammad Moshahid Khan, Junaith S Mohamed, James A Carson, Michael R Deschenes

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
12.0field-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

45 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  3. The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026
    Review
  4. Article
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  12. Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026
    Review
  13. Article
  14. 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
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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

8 authors at 2 institutions in 2 countries.

Stephen E AlwayLaboratory of Muscle Biology and Sarcopenia, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0002-0378-4707
Hector G PaezLaboratory of Muscle Biology and Sarcopenia, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.
Christopher R PitzerLaboratory of Muscle Biology and Sarcopenia, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.
Peter J FerrandiCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.
Mohammad Moshahid KhanCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.
Junaith S MohamedCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.
James A CarsonCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA.
Michael R DeschenesDepartment of Kinesiology, College of William & Mary, Williamsburg, VA, USA.
University of Tennessee Health Science Center · USWilliam & Mary · US

Funding

U.S. Army Medical Research and Development Command, U.S. Department of Defense W81XWH2110187
6 · The paper itself

Abstract

backgroundInjection of exogenous mitochondria has been shown to improve the ischaemia-damaged myocardium, but the effect of mitochondrial transplant therapy (MTT) to restore skeletal muscle mass and function has not been tested following neuromuscular injury. Therefore, we tested the hypothesis that MTT would improve the restoration of muscle function after injury.

methodsBaCl

resultsMTT did not increase systemic inflammation in mice. Muscle mass 7 days following injury was 21.9 ± 2.1% and 17.4 ± 1.9% lower (P < 0.05) in injured as compared with non-injured intra-animal control muscles in phosphate-buffered saline (PBS)- and MTT-treated animals, respectively. Maximal plantar flexor muscle force was significantly lower in injured as compared with uninjured muscles of PBS-treated (-43.4 ± 4.2%, P < 0.05) and MTT-treated mice (-47.7 ± 7.3%, P < 0.05), but the reduction in force was not different between the experimental groups. The percentage of collagen and other non-contractile tissue in histological muscle cross sections, was significantly greater in injured muscles of PBS-treated mice (33.2 ± 0.2%) compared with MTT-treated mice (26.5 ± 0.2%) 7 days after injury. Muscle wet weight and maximal muscle force from injured MTT-treated mice had recovered to control levels by 14 days after the injury. However, muscle mass and force had not improved in PBS-treated animals by 14 days after injury. The non-contractile composition of the gastrocnemius muscle tissue cross sections was not different between control, repaired PBS-treated and repaired MTT-treated mice 14 days after injury. By 21 days following injury, PBS-treated mice had fully restored gastrocnemius muscle mass of the injured muscle to that of the uninjured muscle, although maximal plantar flexion force was still 19.4 ± 3.7% (P < 0.05) lower in injured/repaired gastrocnemius as compared with uninjured intra-animal control muscles.

conclusionsOur results suggest that systemic mitochondria delivery can enhance the rate of muscle regeneration and restoration of muscle function following injury.

Indexed as

Muscular DiseasesRegenerationAnimalsMiceMice, Inbred C57BLMitochondriaMuscle, SkeletalPhosphatesPhosphatesMitochondriaMuscle fibre typesMuscle forceMuscle injuryRegeneration

Identifiers

PMID36604839
PMCPMC9891964
OpenAlexW4313566482

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.