Key Takeaways & Executive Findings
- •• FMRCs enable efficient mitochondrial transfer via magnetic-force-assisted membrane fusion, overcoming limitations of conventional methods. • Transplantation of intact mitochondrial networks from FMRCs restores mitochondrial function in cells with mtDNA depletion or deletion. • Exogenous mitochondria stably and predominantly reside in recipient cells, as confirmed by SNP tracing and qPCR. • FMRC-mediated mitochondrial transplantation reduces mtDNA heteroplasmy by stimulating autophagy and clearance of defective mitochondria.
Abstract
Mitochondrial transplantation is a promising treatment for many diseases associated with mitochondrial defects or aging; however, a reliable method for mitochondrial transfer remains urgently needed. In this study, we assemble fusogenic and magnet-responsive cells (FMRCs), which are enucleated stem cells loaded with Fe3O4 nanoparticles and further incorporated fusogenic vesicular stomatitis virus glycoprotein G (VSV-G). Mitochondrial transplantation from FMRCs via fusion in the presence of a magnetic force restores normal mitotic activity, mitochondrial membrane potential, ROS levels and ATP production in cells subjected to partial mtDNA depletion or in cybrids harboring mtDNA with a 4977-bp deletion. SNP tracing and qPCR analysis of the mitochondrial and nuclear genomes unequivocally demonstrate that exogenous mitochondria are able to reside stably and predominately. Mitochondrial transplantation stimulate autophagy and thus the clearance of defective endogenous counterparts, resulting in lower mtDNA heteroplasmy. These results suggest that FMRCs are excellent vehicles for mitochondrial transplantation and could be used for the treatment of aging and mitochondria-associated diseases.
1. Introduction
Mitochondria are semi-autonomous organelles that generate most of the chemical energy needed to power the cell's biochemical reactions. Mitochondria are also involved in many other fundamental cellular processes [1]. Mutations in mitochondrial DNA (mtDNA) can be Mendelian, maternally inherited, or sporadic and can occur at various time points during development, leading to mitochondrial dysfunction which plays a major role in aging, metabolic diseases, neurodegenerative diseases, neuromuscular disorders and cancers [2–4]. Consequently, mitochondria are now attracting increased research interest and are major targets for pharmaceutical companies.
Mitochondrial transfer offers a potential cure for diseases associated with mitochondrial dysfunction. Mitochondrial transfer has been observed naturally in vivo and in cell culture via open-ended tubular extensions called tunneling nanotubes (TNTs) [5–7]. In addition, membrane-bound extracellular vesicles (EVs) occasionally contain mitochondria and transfer them to surrounding cells [8]. Mitochondrial transfer via TNTs and EVs reportedly decreases reactive oxygen species (ROS) levels and apoptosis rates [9–11]. However, the low efficacy of these approaches limits their therapeutic value.
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Liqun Xu, Xiao Li, Xing Fan, Wei Yan, Wanfei Wu, Junwei Li, Ronghao Deng, Haibao Zhu, Aihua Mao, Pingnan Sun, Xin Zhang, Wencan Xu, Chi-ju Wei (2026). Fabrication of fusogenic and magnet-responsive cells for transplantation of an intact mitochondrial network. Acta Biochimica et Biophysica Sinica. https://doi.org/10.3724/abbs.2026031
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Frequently Asked Questions
What are fusogenic and magnet-responsive cells (FMRCs)?
FMRCs are enucleated stem cells loaded with Fe3O4 nanoparticles and incorporated with fusogenic vesicular stomatitis virus glycoprotein G (VSV-G). They are designed for efficient mitochondrial transfer via membrane fusion enhanced by magnetic force.
How does FMRC-mediated mitochondrial transplantation work?
FMRCs are brought into close proximity with target cells using a magnetic force, facilitating membrane fusion. This allows the transfer of intact mitochondrial networks from FMRCs to recipient cells, restoring mitochondrial function.
What are the key benefits of using FMRCs for mitochondrial transplantation?
FMRCs protect mitochondria from harsh extracellular conditions, enable efficient fusion, and result in stable and predominant residence of exogenous mitochondria. This leads to restored mitotic activity, reduced mtDNA heteroplasmy, and clearance of defective mitochondria via autophagy.
What diseases could benefit from FMRC-based mitochondrial transplantation?
FMRC-based mitochondrial transplantation could be used for treating aging and mitochondria-associated diseases, including metabolic disorders, neurodegenerative diseases, neuromuscular disorders, and cancers.
How is the success of mitochondrial transplantation evaluated in this study?
The study uses SNP tracing and qPCR analysis of mitochondrial and nuclear genomes to confirm stable and predominant residence of exogenous mitochondria. Additionally, functional assays measure mitotic activity, mitochondrial membrane potential, ROS levels, and ATP production.
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