bims-mitrat Biomed News
on Mitochondrial transplantation and transfer
Issue of 2025–09–21
four papers selected by
Gökhan Burçin Kubat, Gulhane Health Sciences Institute



  1. Int J Nanomedicine. 2025 ;20 11169-11196
      Osteoporosis, a global health crisis marked by compromised bone mineral density and heightened fracture susceptibility, demands innovative therapeutic strategies beyond conventional anti-resorptive approaches. Mitochondrial dysfunction, characterized by impaired bioenergetics, oxidative stress overload, and calcium dysregulation, has emerged as a central driver of osteoblast-osteoclast imbalance. Recent breakthroughs in mitochondrial transplantation (MT)-a revolutionary modality involving the transfer of functional mitochondria to metabolically compromised cells-have demonstrated unprecedented efficacy in preclinical osteoporosis models, restoring bone mass, microarchitecture, and mechanical strength. This review synthesizes cutting-edge insights into mitochondrial dynamics in bone homeostasis, dissects the molecular cascades linking mitochondrial failure to osteoporotic pathogenesis, and critically evaluates MT's potential to redefine osteoporosis management. We also discuss novel mechanisms of intercellular mitochondrial trafficking within the osteocyte dendritic network, explore bioengineered delivery platforms (eg, immunomodulatory hydrogels, nanoparticle-encapsulated mitochondria), and address emerging challenges in clinical translation, including donor source optimization, immune compatibility, and CRISPR-engineered mitochondrial genomes. By integrating single-cell omics data and AI-driven mitochondrial viability predictors, this work charts a roadmap for personalized mitochondrial medicine, positioning MT as a cornerstone of next-generation osteoporosis therapeutics.
    Keywords:  mitochondrial disease; mitochondrial transfer; mitochondrial transplantation; osteoporosis
    DOI:  https://doi.org/10.2147/IJN.S537166
  2. Neurodegener Dis Manag. 2025 Sep 19. 1-11
      Parkinson's disease is a neurodegenerative disorder of aging with dopaminergic neuronal degeneration in the substantia nigra leading to motor dysfunction. Mitochondrial dysfunction is central to its pathophysiology, leading to oxidative stress, derangement of energy metabolism, and induction of neuronal apoptosis. Current therapeutic interventions are symptomatic but fail to stop disease progression. Stem cell-based regenerative strategies have been recognized as potential disease-modifying treatments. Mitochondria-augmented stem cell therapy offers a new mechanism for the correction of cellular bioenergetic deficits. Through genetic manipulations or preconditioning protocols, mesenchymal stem cells and induced pluripotent stem cells are engineered to enhance mitochondrial function and transfer. The engineered cells enable delivery of functional mitochondria into damaged neurons through tunneling nanotubes or extracellular vesicles, promoting ATP production, inhibiting reactive oxygen species, and restoring mitophagy. Preclinical models have demonstrated improved neuronal survival and motor function, and novel technologies like CRISPR gene editing and 3D bioprinting offer improved translational relevance.
    Keywords:  Parkinson’s disease; mesenchymal stem cells; mitochondrial dysfunction; mitochondrial transfer; neurorestoration; stem cell therapy
    DOI:  https://doi.org/10.1080/17582024.2025.2562741
  3. Bone Joint Res. 2025 Sep 19. 14(9): 805-819
       Aims: Mitochondrial transplantation has been proposed as a potential treatment for injured ligament tissue. This study aimed to investigate the relationship between the time from injury to surgery and the activity of injured anterior cruciate ligament (ACL) cells. Additionally, we evaluated the effectiveness of mitochondrial transplantation in chronically injured ACL cells and in an in vivo ACL partial tear animal model.
    Methods: First, ACL injured tissue from rabbits (n = 6 for each timepoint) was harvested at two (acute), four (subacute), and eight (chronic) weeks following ACL transection. We investigated cell proliferation, migration capability, and the expression of collagen synthesis, vascular endothelial growth factor (VEGF), and transforming growth factor-β (TGF-β) genes in injured ACL cells at different injury timepoints. Second, we isolated mitochondria from human adipose-derived stem cells (hADSCs) and transplanted them into the ACL cells. Lastly, we evaluated the in vivo effects of hADSCs-mitochondrial transplantation in a rabbit knee model with partial ACL tear.
    Results: After injury, the highest cell activity was observed at four weeks. Immunohistochemical staining showed that hADSCs-mitochondria were taken up by the eight-week injured ACL cells, leading to subsequent improvements in cell viability, migration capability, and collagen synthesis, and VEGF gene expression which were superior to those of untreated cells. At eight weeks, treated injured ACL cells achieved cell proliferation and collagen type I, type III, and VEGF expression levels comparable to those of four-week injured cells. In the in vivo study, enhanced collagen synthesis was observed in the histological analysis following hADSCs-mitochondrial transplantation.
    Conclusion: The optimal timing of ACL reconstruction is four to six weeks after injury due to peak cell activity. Mitochondrial transplantation improves the activity of chronically injured ACL cells and enhances collagen synthesis in ACL partial tears, highlighting its potential as a treatment for improving their regenerative capability.
    DOI:  https://doi.org/10.1302/2046-3758.149.BJR-2025-0186
  4. Theranostics. 2025 ;15(17): 9279-9293
      Rationale: Mitochondrial dysfunction in ovarian granulosa cells (GCs) and cumulus cells (CCs) is a defining feature of reproductive aging, contributing to impaired oocyte quality and reduced fertility. This study investigates whether enhancing cytoskeletal dynamics or promoting structural contact between cells can restore mitochondrial function and mitigate ovarian aging. Methods: Mitochondrial exchange was assessed using co-culture systems, live-cell imaging, and mitochondrial labeling in human ovarian somatic cells. Cytoskeletal modulation was achieved using FTY720, and cell-cell contact was enhanced through soft 3D extracellular matrix (ECM) scaffolds. Functional outcomes were evaluated through ATP assays, mitochondrial membrane potential, Seahorse bioenergetics profiling, and transcriptomic analysis. In vivo validation was conducted in aged mice treated with FTY720. Results: Granulosa and cumulus cells exchanged mitochondria via tunneling nanotubes (TNTs), a process significantly reduced with age. Mitochondrial transfer was contact-dependent and not mediated by paracrine signaling. FTY720 enhanced TNT formation and mitochondrial delivery, restoring ATP levels, membrane potential, and oxidative phosphorylation in aged cells. 3D ECM culture promoted spheroid formation, activated YAP signaling, and improved mitochondrial function without pharmacological agents. In aged mice, FTY720 treatment increased follicle numbers, improved oocyte mitochondrial quality, and elevated serum AMH levels. Conclusions: These findings demonstrate that somatic cell contact is essential for mitochondrial complementation in aging ovaries. By promoting intercellular connectivity through cytoskeletal or microenvironmental remodeling, endogenous mitochondrial sharing can be reactivated to restore bioenergetic function. This approach offers a novel regenerative strategy to counteract reproductive aging.
    Keywords:  Cell-cell communication; Mitochondrial transfer; Ovarian aging; Reproductive microenvironment
    DOI:  https://doi.org/10.7150/thno.119957