bims-mitrat Biomed News
on Mitochondrial transplantation and transfer
Issue of 2025–11–02
four papers selected by
Gökhan Burçin Kubat, Gulhane Health Sciences Institute



  1. Nat Commun. 2025 Oct 27. 16(1): 9448
      Mitochondria transfer is a spontaneous process that releases functional mitochondria to damaged cells via different mechanisms including extracellular vesicle containing mitochondria (EV-Mito) to restore mitochondrial functions. However, the limited EV-Mito yield makes it challenging to supply a sufficient quantity of functional mitochondria to damaged cells, hindering their application in mitochondrial diseases. Here, we show that the release of EV-Mito from mesenchymal stem cells (MSCs) is regulated by a calcium-dependent mechanism involving CD38 and IP3R signaling (CD38/IP3R/Ca2+ pathway). Activating this pathway through our non-viral gene engineering approach generates super donor MSCs which produce Super-EV-Mito with a threefold increase in yield compared to Ctrl-EV-Mito from normal MSCs. Leber's hereditary optic neuropathy (LHON), a classic mitochondrial disease caused by mtDNA mutations, is used as a proof-of-concept model. Super-EV-Mito rescues mtDNA defects and alleviates LHON-associated symptoms in LHON male mice. This strategy offers a promising avenue for enhancing mitochondria transfer efficiency and advancing its clinical application in mitochondrial disorders.
    DOI:  https://doi.org/10.1038/s41467-025-64486-9
  2. Stem Cell Res Ther. 2025 Oct 28. 16(1): 585
       BACKGROUND: Mitochondrial dyshomeostasis plays an important role in neuronal damage after cerebral ischemia-reperfusion, and Miro1 is a core protein that regulates mitochondrial homeostasis. In this study, we aimed to investigate the neuroprotective effects of bone marrow-derived mesenchymal stem cells (BMSCs) via mitochondrial homeostasis in rats after cardiac arrest (CA), and to clarify the role that the protein Miro1 plays in this protective efficacy.
    METHODS: The study compared the effects of BMSCs in which Miro1 was overexpressed BMSCs (BMSCs-mirohi), knocked down (BMSCs-mirolo), and unmodified BMSCs on mitochondrial homeostasis in hippocampal neurons to evaluate their neuroprotective effects of these cells in a rat model of global cerebral ischemia-reperfusion injury. Rats underwent CA modeling for 5 min and received cardiopulmonary resuscitation (CPR). Two hours after the restoration of spontaneous circulation, 1 mL of PBS or 1 mL containing 1 × 106 BMSCs (normal, mirohi, or mirolo) were injected via the femoral vein. The neurological function of rats was assessed based on Neurological Disability Score (NDS) values. Brain histopathological examination was conducted to evaluate brain injury by measuring oxidative stress levels and the apoptosis rate of hippocampal neurons. Immunoblotting and transmission electron microscopy were applied to detect the expression of mitophagy-related proteins in hippocampal neurons. Immunofluorescence was used to track the mitochondria in BMSCs and observe mitochondrial transfer. Additionally, the membrane potential level, oxidative stress level, and ATP content of mitochondria in hippocampal neurons were measured to assess the impact of transplanted BMSCs on mitochondrial quality in these hippocampal neurons.
    RESULTS: Immunofluorescence staining revealed the presence of mitochondria from MitoTracker-labeled BMSCs in rat hippocampal neurons post-CPR. Additionally, the fluorescence intensity of TOMM20 was notably increased following the transplantation of BMSCs. Through immunoblotting experiments, we identified that BMSCs amplified the post-CPR protein expression of LC3, p62, PINK1 and parkin in hippocampal neurons. The number of autophagosomes significantly increased in hippocampal neurons following BMSC transplantation, as observed through transmission electron microscopy. Flow cytometry, Hematoxylin and Eosin (HE) staining, and NDS scoring indicated that BMSCs effectively reduced reactive oxygen species accumulation in hippocampal neurons and mitochondria after CPR. Furthermore, they restored mitochondrial membrane potential and ATP levels in the hippocampus while decreasing apoptosis, ultimately contributing to the restoration of neurological function. Additionally, unlike BMSCs-mirolo, BMSCs-mirohi were able to significantly enhance the efficiency of BMSC-mediated mitochondrial transfer and enhance mitophagy. This amplification, in turn, was found to bolster the protective impact of BMSCs on hippocampal neurons during CPR, thereby contributing to the restoration of rat neurological function.
    CONCLUSIONS: These analyses revealed that BMSC transplantation has a dual protective effect by facilitating healthy mitochondrial transfer and promoting the autophagic degradation of damaged mitochondria, effectively enhancing hippocampal neuronal mitochondrial function following CA while reducing neuronal apoptosis, restoring neuronal function, and alleviating neuropathological damage. Moreover, Miro1 can enhance the efficiency of mitochondrial transfer and promote BMSC-mediated mitophagy induction, thereby optimizing the therapeutic effect of BMSCs.
    Keywords:  Bone marrow-derived mesenchymal stem cells; Cardiopulmonary resuscitation; Miro1; Mitochondria
    DOI:  https://doi.org/10.1186/s13287-025-04724-5
  3. Redox Biol. 2025 Oct 17. pii: S2213-2317(25)00415-X. [Epub ahead of print]88 103902
      Mitochondrial transplantation is an upcoming therapeutic modality where transfer of healthy robust mitochondria bio-enhances metabolically dysfunctional cells or tissues. Though the concept of MT germinated in early 1980s in a bid to develop antibiotic resistance between cells, this innovative treatment has since undergone various breakthroughs in addressing metabolic dysfunction in various systemic diseases. Four decades since its advent, MT is now being applied in the field of Ophthalmology, where metabolic disorders affecting various ocular tissues contribute significantly to disease pathogenesis. Encouraged by the success of MT in other organs such as heart, lung and brain, this therapy has recently been applied to ocular disorders. MT is an emerging ocular therapy, with promising therapeutic outcomes for corneal, optic nerve, and retinal disorders. However, before it can be adopted as a "bench to bedside" therapy for ocular disorders, MT faces several potential bottlenecks. This review provides an overview of mitochondrial biology in eye diseases, summarizes the current state-of-the-art in ocular MT, whilst discussing challenges and future direction of bringing MT into clinical practice.
    Keywords:  Bioenergetic rescue; Clinical translation; Mitochondria transplantation; Mitochondrial biology; Ocular metabolic diseases; Oxidative stress
    DOI:  https://doi.org/10.1016/j.redox.2025.103902
  4. Zhonghua Shao Shang Yu Chuang Mian Xiu Fu Za Zhi. 2025 Oct 20. 41(10): 937-948
      Objective: To explore the effects of mitochondrial transplantation on full-thickness skin defects in diabetic rats. Methods: This study was an experimental study. Functionally intact mitochondria were extracted from the liver tissue of 6-8-week-old male Sprague Dawley rats (the same age and sex below). Mouse L929 cells and human umbilical vein endothelial cells (HUVECs) were cultured in medium containing high-glucose (50 mmol/L) for 24 hours to induce high-glucose injury. According to the random number table method (the same grouping method below), they were then divided into control group (Ctrl group, treated with conventional medium), growth factor group (GF group, treated with medium containing 20 U/mL recombinant human epidermal growth factor), and mitochondrial group (Mito group, treated with medium containing 12.5 μg/mL exogenous mitochondria). The scratch assay was performed to evaluate the migration rate of mouse L929 cells at 6 hours after scratching (n=3). The length and number of branch nodes of tube formed by HUVECs were measured after 2 and 6 hours of culture (n=3). After 24 hours of culture, the reactive oxygen species (ROS) levels and mitochondrial membrane potential in aforemetioned two types of cells were detected according to the kit instructions (n=6). Eighteen Sprague Dawley rats were selected and a type 1 diabetic rat model was successfully established. Then, the full-thickness skin defects with a diameter of 1 cm were created on their backs. The rats were divided into Ctrl group, GF group, and Mito group (with each group of 6 rats). At post-injury days (PID) 0 (immediately), 3, and 6, the wounds were subcutaneously injected with normal saline (Ctrl group), topically sprayed with an equal amount of rhEGF solution at a dose of 40 U/cm² (GF group), or subcutaneously injected with equal amount of mitochondrial suspension at a dose of 5 μg/g (Mito group), respectively. The percentage of remaining wound area of rats was calculated at PID 3, 6, and 12. At PID 12, the epithelialization and collagen deposition in the wound of rats were detected by hematoxylin and eosin staining and Masson's staining, respectively. Immunofluorescence staining was used to detect the expression of CD31 (a marker for neovascularization) and neurofilament 200 (a marker for nerves) in the wound of rats. The ROS levels, number of apoptotic cells, ATP content in the wound of rats were detected according to the kit instructions. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in the wound of rats were detected by enzyme-linked immunosorbent assay. Results: At 6 hours after scratching, compared with that in Ctrl group, the migration rate of mouse L929 cells in GF group was significantly increased (P<0.05). compared with that in GF group, the migration rate of mouse L929 cells in Mito group was significantly increased (P<0.05); After 2 and 6 hours of culture, compared with those in Ctrl group, the numbers of branch nodes and the lengths of tube formed by HUVECs in both GF group and Mito group were significantly increased (P<0.05). Compared with those in GF group, the numbers of branch nodes and the lengths of tube formation of HUVECs after 2 and 6 hours of culture in Mito group were significantly increased (P<0.05). After 24 hours of culture, compared with those in Ctrl group, the ROS levels in both mouse L929 cells and HUVECs in GF group and Mito group were significantly decreased (P<0.05), while the mitochondrial membrane potentials were significantly increased (P<0.05); compared with those in GF group, the ROS levels in both mouse L929 cells and HUVECs in Mito group were significantly decreased (P<0.05), while the mitochondrial membrane potentials were significantly increased (P<0.05). At PID 3, 6, and 12, the percentages of remaining wound area of rats in Mito group ((46±3)%, (37±3)%, (18±3)%) were significantly lower than those in Ctrl group ((71±4)%, (63±4)%, (47±5)%) and GF group((62±3)%, (54±3)%, (33±4)%), P<0.05. At PID 12, in the wounds of rats in Mito group, the status of epithelialization and collagen deposition, as well as the conditions of angiogenesis and nerve repair, were superior to those in growth factor and control groups. Compared with those in Ctrl group, the ROS levels and number of apoptotic cells in the wounds of rats in GF group and Mito group were significantly decreased (P<0.05), the ATP content significantly increased (P<0.05), and the levels of TNF-α, IL-1β, and IL-6 were all significantly reduced (P<0.05). Compared with those in GF group, the ROS levels and number of apoptotic cells in the wounds of rats in Mito group were significantly decreased (P<0.05), the ATP content significantly increased (P<0.05), and the levels of TNF-α, IL-1β, and IL-6 were all significantly reduced (P<0.05). Conclusions: Mitochondrial transplantation enhances mitochondrial ATP production and reduces the level of oxidative stress in cells under high-glucose injury, which improves the migration capacity of mouse L929 cells and the angiogenesis capacity of HUVECs. Simultaneously, it facilitates epithelialization and collagen deposition in full-thickness skin defect wounds of diabetic rats, reduces the levels of inflammatory cytokines, and inhibits cell apoptosis, thereby accelerating wound healing.
    DOI:  https://doi.org/10.3760/cma.j.cn501225-20250721-00315