ReviewJournal of translational medicine2026
Targeting the mitochondrial metabolite-dynamics-MDVs-MitoEVs axis: a new frontier in osteoarthritis management.
Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteoarthritis (OA) is characterized by progressive cartilage degradation, osteophyte formation, and synovitis. OA progression is linked to mitochondrial metabolic dysfunction, marked by tricarboxylic acid (TCA) cycle imbalance and impaired oxidative phosphorylation (OXPHOS). KEY SCIENTIFIC CONCEPTS OF REVIEW: Three critical factors regulate mitochondrial metabolism: mitochondrial metabolites, mitochondrial dynamics, and mitochondrial-derived vesicles (MDVs). Mitochondrial metabolites such as fumarate and succinate exacerbate OA pathogenesis by mediating mitochondrial dysfunction, whereas itaconate, α-ketoglutarate (α-KG), and fumarate derivatives confer protective effects. Imbalanced mitochondrial dynamics drive cartilage degradation through oxidative stress. Inflammatory MDVs may accelerate OA by transferring mitochondrial damage-associated molecular patterns (mtDAMPs) into the extracellular space through mitochondrial-derived extracellular vesicles (mitoEVs). Given the interplay of mitochondrial metabolites, mitochondrial dynamics, and MDVs/mitoEVs, we propose that the metabolite-dynamics-MDVs-mitoEVs axis represents a pivotal mechanism driving OA progression and a potential target for mitochondrial-directed therapies.
conclusionFuture efforts should prioritize advancing mitochondrial metabolic modulators and MSC-mitoEVs, with validation through synovial fluid biomarkers and support from crucial preclinical safety and delivery studies.
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Registered trials
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.