bims-mitrat Biomed News
on Mitochondrial transplantation and transfer
Issue of 2026–03–29
four papers selected by
Gökhan Burçin Kubat, Başkent Üni̇versi̇tesi̇



  1. J Adv Res. 2026 Mar 20. pii: S2090-1232(26)00257-2. [Epub ahead of print]
       BACKGROUND: Current therapeutic models for ischemic stroke (IS) are shifting from a narrow focus on neuroprotection to a broader concept of cytoprotection. This new paradigm emphasizes rescuing damaged brain cells and maintaining their structural and functional integrity through organelle transfer between healthy and damaged cells. Mounting evidence have supported that intracellular mitochondrial transfer is an intrinsic response to IS, playing a critical role in mitigating neural damage. Consequently, mitochondrial transplantation from stem cell is emerging as a therapeutic avenue for IS.
    AIM OF REVIEW: This article reviews the IS-induced mitochondrial dysfunction, the modes and mechanisms of endogenous intracellular mitochondrial transfer, and recent advances in using stem cell-derived mitochondrial transplantation to treat IS.
    KEY SCIENTIFIC CONCEPTS: This review emphasizes the dual roles of mitochondrial transfer in determining neural cells fate and neurological function recovery following IS. On one hand, health cells can donate intact mitochondria to damaged cells, to revitalize them by restoring cell metabolic function. On the other hand, damaged cell may expel dysfunction mitochondria, which can be cleared by healthy neighbors or, alternatively propagate injury. We discuss the current challenges in this field and propose that enhancing healthy mitochondrial transfer or preventing damaged mitochondrial release may hold great potential for alleviating IS injury.
    Keywords:  Cell to cell communication; Ischemic stroke; Mitochondrial transfer; Preserving neuronal function; Stem cell therapy
    DOI:  https://doi.org/10.1016/j.jare.2026.03.037
  2. Biology (Basel). 2026 Mar 23. pii: 513. [Epub ahead of print]15(6):
      From bacteria to higher vertebrates, cells have developed different systems to communicate with each other and transmit specific signals in a dynamic interplay with neighborhood cells. This review focuses on cell-to-cell communication mediated by nanotubes, membrane protrusions present during evolution from bacteria to higher plants and animals. We describe the basic structure of nanotubes in different organisms and cell types and their functions, which cover transfer of signaling molecules, ions, organelles and pathogens in a cell- and context-dependent manner, thereby promoting cell survival, tissue development, response to stress, pathogens' spreading and drug resistance. We also provide an overview of recent studies that are broadening our understanding of the role of these conduits in the pathogenesis of high-incidence diseases in humans, such as cancer and neurodegeneration.
    Keywords:  bacterial nanotubes; cytonemes; dendritic nanotubes; mitochondrial transfer; plasmodesmata; septal pores; tunneling nanotubes
    DOI:  https://doi.org/10.3390/biology15060513
  3. J Funct Biomater. 2026 Mar 02. pii: 119. [Epub ahead of print]17(3):
      Achilles tendon rupture often leads to poor functional recovery due to limited self-healing, with mitochondrial dysfunction in tendon stromal cells (TSCs) being a key factor in disease progression. Here, we developed adipose-derived stromal cell (ADSC) membrane-coated mitochondria (Mito-NPs) to target this dysfunction and evaluate their therapeutic potential for tendon repair. Mito-NPs exhibited uniform size, stable surface charge, and effective membrane coating. In lipopolysaccharide-induced inflammatory TSCs, Mito-NPs enhanced oxidative phosphorylation, improved mitochondrial metabolic homeostasis, and reshaped gene expression profiles to normalize TSC functional phenotypes, including inflammation, migration, and collagen synthesis. When encapsulated in a reactive oxygen species (ROS)-responsive hydrogel (Mito-NPs@HG) and implanted into rat Achilles tendon injuries, Mito-NPs@HG improved gait function, decreased local inflammation, and promoted histological repair of damaged tendons by enhancing collagen organization and reducing inflammation. Our findings demonstrate that ADSC membrane-coated mitochondria effectively rescue TSC dysfunction and facilitate tendon regeneration, providing a promising translational strategy for treating tendon injuries.
    Keywords:  membrane-coated nanoparticles; metabolic modulation; mitochondrial delivery; oxidative phosphorylation; tendon repair
    DOI:  https://doi.org/10.3390/jfb17030119
  4. Biotechniques. 2026 Jan-Dec;78(1-12):78(1-12): 1-11
      Mitochondria, with their own DNA, Represent a potential target for nucleic acid-based precision therapies. However, effective delivery of therapeutic oligonucleotides remains challenging due to the dual mitochondrial membranes and the localization of mitochondrial DNA within nucleoid complexes in the matrix. To understand the delivery process and assess the delivery efficiency of potential vectors, such as dendrimers, it is essential to effectively quantify the oligonucleotides that are successfully delivered to and remain within mitochondria. Currently, there are only limited yet inconvenient methods available for this purpose. Here, we describe a method for quantifying the delivery of fluorescent oligonucleotide cargos in isolated mitochondria using a microfiltration apparatus for reliable fluorescent analysis. By working within a range of dilutions, we are able to safeguard the concentration limits. The quantification protocol also enables the visualization of specific localization within mitochondria, allowing for the determination of whether delivery can occur across both membranes. This is particularly useful, as it offers a key insight into improving vectors as they must deliver the cargoes within the mitochondrial matrix. We validate this method in this proof-of-concept study, providing biological data to assess the difference between two amphiphilic dendrimer vectors for oligonucleotide delivery in mitochondria.
    Keywords:  Oligonucleotide delivery; dendrimers; microfiltration; mitochondria; subcellular localization
    DOI:  https://doi.org/10.1080/07366205.2026.2635461