Evidence map›Paper›PMID 37209146›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2023

Mitochondrial transplantation as a possible therapeutic option for sarcopenia.

Ibrahim Turkel, Berkay Ozerklig, Merve Yılmaz, Oner Ulger, Gokhan Burcin Kubat, Meltem Tuncer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
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  9. Review
  10. Skeletal muscle dysfunction in amyotrophic lateral sclerosis: a mitochondrial perspective and therapeutic approaches.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Mitochondrial transplantation and transfer: The promising method for diseases.Turkish journal of biology = Turk biyoloji dergisi · 2023
    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

6 authors at 3 institutions in 1 country.

Ibrahim TurkelDepartment of Exercise and Sport Sciences, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey.
Berkay OzerkligDepartment of Exercise and Sport Sciences, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey.
Merve YılmazDepartment of Medical Biochemistry, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Oner UlgerDepartment of Mitochondria and Cellular Research, Health Sciences Institute, Health Sciences University, Ankara, Turkey.
Gokhan Burcin KubatDivision of Sport Sciences and Technology, Institute of Health Sciences, Hacettepe University, Ankara, Turkey. gokhankubat@hacettepe.edu.tr.ORCID 0000-0003-3220-465X
Meltem TuncerDepartment of Physiology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Hacettepe University · TRAnkara University · TRSağlık Bilimleri Üniversitesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With advancing age, the skeletal muscle phenotype is characterized by a progressive loss of mass, strength, and quality. This phenomenon, known as sarcopenia, has a negative impact on quality of life and increases the risk of morbidity and mortality in older adults. Accumulating evidence suggests that damaged and dysfunctional mitochondria play a critical role in the pathogenesis of sarcopenia. Lifestyle modifications, such as physical activity, exercise, and nutrition, as well as medical interventions with therapeutic agents, are effective in the management of sarcopenia and offer solutions to maintain and improve skeletal muscle health. Although a great deal of effort has been devoted to the identification of the best treatment option, these strategies are not sufficient to overcome sarcopenia. Recently, it has been reported that mitochondrial transplantation may be a possible therapeutic approach for the treatment of mitochondria-related pathological conditions such as ischemia, liver toxicity, kidney injury, cancer, and non-alcoholic fatty liver disease. Given the role of mitochondria in the function and metabolism of skeletal muscle, mitochondrial transplantation may be a possible option for the treatment of sarcopenia. In this review, we summarize the definition and characteristics of sarcopenia and molecular mechanisms associated with mitochondria that are known to contribute to sarcopenia. We also discuss mitochondrial transplantation as a possible option. Despite the progress made in the field of mitochondrial transplantation, further studies are needed to elucidate the role of mitochondrial transplantation in sarcopenia. KEY MESSAGES: Sarcopenia is the progressive loss of skeletal muscle mass, strength, and quality. Although the specific mechanisms that lead to sarcopenia are not fully understood, mitochondria have been identified as a key factor in the development of sarcopenia. Damaged and dysfunctional mitochondria initiate various cellular mediators and signaling pathways, which largely contribute to the age-related loss of skeletal muscle mass and strength. Mitochondrial transplantation has been reported to be a possible option for the treatment/prevention of several diseases. Mitochondrial transplantation may be a possible therapeutic option for improving skeletal muscle health and treating sarcopenia. Mitochondrial transplantation as a possible treatment option for sarcopenia.

Indexed as

SarcopeniaHumansMitochondriaMuscle, SkeletalQuality of LifeMitochondrial dysfunctionMitochondrial transplantationSarcopeniaSkeletal muscle

Identifiers

PMID37209146
OpenAlexW4377140233

What OpenQuestion holds

Textmetadata
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.