Evidence map›Paper›PMID 40354767›Full record

ReviewRedox biology2025

Targeting mitochondria in bone and cartilage diseases: A narrative review.

Daniel H Mendelsohn, Nike Walter, Wing-Hoi Cheung, Ronald Man Yeung Wong, Rebecca Schönmehl, Lina Winter, Thaqif El Khassawna, Christian Heiss, Christoph Brochhausen, Markus Rupp

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  20. What's New in Musculoskeletal Basic Science.The Journal of bone and joint surgery. American volume · 2025
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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

10 authors.

Daniel H MendelsohnInstitute of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Friedrich-Baur-Institute, Department of Neurology, LMU Clinic Munich, Germany.
Nike WalterDepartment of Psychosomatic Medicine, University Medical Center Regensburg, Regensburg, Germany.
Wing-Hoi CheungDepartment of Orthopedics and Traumatology, The Chinese University of Hong Kong, Hong Kong Special Administrative Region of China.
Ronald Man Yeung WongDepartment of Orthopedics and Traumatology, The Chinese University of Hong Kong, Hong Kong Special Administrative Region of China.
Rebecca SchönmehlInstitute of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Lina WinterInstitute of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Thaqif El KhassawnaExperimental Trauma Surgery, Justus-Liebig-University Giessen, Germany.
Christian HeissDepartment of Trauma, Hand and Reconstructive Surgery, University Hospital Giessen, Germany; Biruni University, Istanbul, Türkiye.
Christoph BrochhausenInstitute of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Markus RuppDepartment of Trauma, Hand and Reconstructive Surgery, University Hospital Giessen, Germany. Electronic address: markus.rupp@chiru.med.uni-giessen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are essential regulators of bone health, controlling cell differentiation, cellular energy production, immune function, osteogenesis, and osteoclast activity. Their dysfunction is linked to orthopedic disorders such as osteoporosis, osteoarthritis, and osteomyelitis, contributing to impaired bone homeostasis and increased fracture risk. While mitochondrial research has been more advanced in fields such as cardiology and neurology, emerging therapeutic strategies from these areas are beginning to show potential for translation into orthopedics. These include mitochondrial biogenesis stimulation, mitochondrial fission inhibition, antioxidant therapies, mitochondrial transplantation, and photobiomodulation, which have demonstrated success in enhancing tissue repair, reducing oxidative stress, and improving overall cellular function in non-orthopedic applications. The novel inhibitor of mitochondrial fission and accumulation of reactive oxygen species Mdivi-1 offers potential to improve clinical outcomes of bone diseases by alleviating cellular dysfunction and preventing bone loss. While these treatments are still in the developmental phase, they present innovative approaches to address mitochondrial dysfunction in orthopedic conditions, potentially transforming bone disease management and enhancing patient outcomes. This report explores research regarding the involvement of mitochondrial health in bone and joint function and discusses possible future treatment strategies targeting mitochondria in orthopedic conditions.

Indexed as

Bone DiseasesCartilage DiseasesMitochondriaAnimalsBone and BonesHumansMitochondrial DynamicsOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesBoneCartilageMitochondriaMitochondrial dynamicsOsteoarthritisOsteomyelitisOsteoporosis

Identifiers

PMID40354767
PMCPMC12136924

What OpenQuestion holds

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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.