bims-mitrat 2026-03-08 papers

bims-mitrat

Biomed News

on Mitochondrial transplantation and transfer

Issue of 2026–03–08
five papers selected by
Gökhan Burçin Kubat, Başkent Üni̇versi̇tesi̇

The landscape of mitochondrial transplantation: A bibliometric analysis.
Mitochondrial transfer and transplantation in the immune cells: Mechanistic foundations, medical applications, and future prospects.
Mesenchymal stem cell mitochondrial transfer effectively protects Leber's Hereditary Optic Neuropathy (LHON) mutant cells from mitochondrial damage.
Characterization of a UQCRC1 variant in a patient with progressive weakness, pain and sleep issues reveals a functional mitochondrial defect restored by mitochondrial transplantation.
Mitochondrial-Derived Vesicles: An Emerging Whisperer in Neurological Disorders.

Cell Transplant. 2026 Jan-Dec;35:35 9636897261427903

The landscape of mitochondrial transplantation: A bibliometric analysis.

Xiaojuan Yang, Miaohui Wang, Xuhang Fan, Minheng Zhang, Siyao Chen, Yue Liu, Haixia Fan.

  Recent years have witnessed rapid progress in mitochondrial transplantation (MT) as a novel strategy for restoring mitochondrial function in diverse pathological conditions, including somatic mitochondrial transfer and reproductive mitochondrial replacement therapy. With its expanding applications in regenerative medicine and disease modeling, systematic quantitative evaluation of the global MT research landscape remains limited. To address this gap, we performed a bibliometric analysis of publications indexed in the Web of Science Core Collection from 1996 to 2024, with cross-database validation using Scopus. CiteSpace, VOSviewer, and the R package bibliometrix were applied to assess publication trends, collaboration networks, co-citation patterns, and keyword co-occurrence. In total, 1104 articles and reviews were included. The results revealed rapid growth in MT-related research, with the United States and China as leading contributors. Mitochondrion emerged as the most influential journal, while Yamada Y, Harashima H, and McCully JD were recognized as key authors. High-frequency keywords highlighted major themes including mitochondrial transfer, mesenchymal stem cells, and ischemia-reperfusion injury. Emerging terms such as extracellular vesicles, tunneling nanotubes, and advanced delivery systems, particularly the MITO-Porter platform, reflected current research frontiers. Overall, this study provides a comprehensive overview of global research trends and evolving directions in mitochondrial transplantation.

Keywords:  MITO-porter; cardiovascular diseases; mitochondrial dysfunction; mitochondrial transplantation; neurodegenerative diseases; stem cells; therapeutic applications

DOI:  https://doi.org/10.1177/09636897261427903
Autoimmun Rev. 2026 Feb 28. pii: S1568-9972(26)00025-X. [Epub ahead of print]25(3): 104011

Mitochondrial transfer and transplantation in the immune cells: Mechanistic foundations, medical applications, and future prospects.

Xiaofeng Liu, Xinyu Feng, Deping Zhan, Heng Yin.

  Mitochondria exhibit tissue-specific physiological functions and are central to the maintenance of cellular homeostasis. Emerging evidence indicates that intercellular mitochondrial transfer is regulated by multiple determinants and exerts a profound influence on the function of both innate and adaptive immune cells. The underlying mechanisms are highly heterogeneous, involving distinct cellular contexts, microenvironmental cues, and modes of intercellular communication. This review summarizes the major triggers and mechanistic pathways governing mitochondrial transfer in immune cells and immune-related diseases, and discusses the therapeutic potential of this process while highlighting key challenges that currently limit its clinical translation. By integrating recent mechanistic insights and translational perspectives, this review aims to provide a conceptual framework for the development of mitochondrial transfer-based strategies in the treatment of immune-mediated disorders.

Keywords:  Immune cells; Mitochondrial transfer; Neutrophils; T cells

DOI:  https://doi.org/10.1016/j.autrev.2026.104011
Acta Histochem. 2026 Feb 28. pii: S0065-1281(26)00016-4. [Epub ahead of print]128(2): 152331

Mesenchymal stem cell mitochondrial transfer effectively protects Leber's Hereditary Optic Neuropathy (LHON) mutant cells from mitochondrial damage.

Aswathy P Nair, Aishwarya Janaki P, Janani Gopalarethinam, Abishek Kumar B, Balachandar Vellingiri, Mohana Devi Subramaniam.

  Leber's Hereditary Optic Neuropathy (LHON) is the most prevalent mitochondrial inherited disorder, primarily caused by primary mitochondrial mutations. Clinically, LHON is characterized by degeneration of optic nerves that leads to acute or subacute sudden or painless central vision loss. Currently no effective treatment has been established for LHON. Recent studies have highlighted the significance of intercellular mitochondrial transfer, which facilitates communication between cells and presents a novel therapeutic avenue. In this study, we investigated the formation of tunnelling nanotubes (TNTs) and the subsequent mitochondrial transfer between Bone Marrow Mesenchymal Stem Cells (BM-MSCs) and LHON ND4 mutant cells within the coculture system. Our findings demonstrated that mitochondrial transfer from BM-MSCs to LHON mutant cells via TNTs effectively rescued the mutant LHON cells by reducing apoptosis, restoring mitochondrial membrane potential and reducing reactive oxygen species (ROS) generation. These results provide compelling evidence of cell-cell communication between mesenchymal stem cells and LHON mutant cells, indicating a potential regenerative capacity through the reduction in mitochondrial mutation load. This study would help to implement further research in this area for the protective effect of mitochondria transfer and future cell-based treatment approaches for LHON.

Keywords:  Leber’s Hereditary Optic Neuropathy; Mitochondria transfer; Mitochondrial disease; Stem cells; Tunneling Nanotubes

DOI:  https://doi.org/10.1016/j.acthis.2026.152331
Mol Genet Metab Rep. 2026 Mar;46 101302

Characterization of a UQCRC1 variant in a patient with progressive weakness, pain and sleep issues reveals a functional mitochondrial defect restored by mitochondrial transplantation.

Gerardo G Piroli, Rebecca Myers, Lynda Holloway, Andrew Hayek, Ellen Linebaugh, Julie R Jones, Cindy Skinner, Steven A Skinner, Norma Frizzell, Richard Steet.

  Primary mitochondrial defects underlie the heterogeneity of many rare inherited disorders. Pathogenic variants that disrupt the function of the multi-subunit protein complexes of the mitochondrial respiratory chain contribute to a range of neurological phenotypes and other clinical manifestations. These variants are also thought to contribute to the onset and progression of numerous more common neurodegenerative conditions such as Parkinson's and Alzheimer's disease. Here we describe an individual affected with progressive muscle weakness and pain harboring a paternally inherited missense variant in UQCRC1, encoding a subunit of Complex III. Biochemical characterization of cells from the proband and his father demonstrated normal steady-state levels of UQCRC1 and UQCRC2 protein. Functional assessment of mitochondrial respiration in lymphoblasts and fibroblasts, however, showed a clear deficit in respiratory parameters in the proband, with a more attenuated response in the father. Lastly, we demonstrate that healthy mitochondria isolated from HEK293 cells can be transferred to the patient lymphoblasts, restoring basal mitochondrial respiration and ATP production. Perspectives on the contribution of this variant to the patient phenotypes, and the potential of mitochondrial transplantation and different compounds as treatment modalities for patients with primary mitochondrial deficits, is discussed.

Keywords:  Complex III; Mitochondria; Mitochondrial transplantation; Respiration; UQCRC1; UQCRC2

DOI:  https://doi.org/10.1016/j.ymgmr.2026.101302
Eur J Neurosci. 2026 Mar;63(5): e70449

Mitochondrial-Derived Vesicles: An Emerging Whisperer in Neurological Disorders.

Nermeen Z Abuelezz, Fayza Eid Nasr, Amira Emad Abd El Aziz, Mariam K Ahmed, Nesrine S El Sayed.

  Mitochondrial dysfunction is a pivotal feature in the pathogenesis of various neurological and neurodegenerative disorders. The brain, with its high metabolic demands, is particularly vulnerable to impaired mitochondrial function, leading to oxidative stress, disturbed calcium homeostasis, and hyperactivated microglial responses. Mitochondrial disturbances majorly contribute to neuronal damage, synaptic dysfunction, and cognitive decline, making mitochondria a crucial target for therapeutic intervention in brain disorders. In this context, mitochondrial-derived vesicles (MDVs) are increasingly emerging as a novel aspect of mitochondrial biology with significant implications for brain health and disease. Prior to mitophagy, MDVs are released from stressed mitochondria, incorporating either healthy or damaged mitochondrial components as an earlier defense mechanism to maintain mitochondrial integrity and homeostasis. Furthermore, MDVs contribute to intercellular communication and extracellular neuroinflammation signaling, potentially influencing the progression of neurological disorders. This review provides a thorough overview of MDVs' subpopulations, highlighting the most recently reported MDVs roles across multiple neurological disorders and exploring their potential in diagnostic and therapeutic settings. Additionally, we further analyze the current limitations that hinder broader clinical applications of MDVs and present future perspectives and key recommendations to overcome these obstacles, aiming to enhance their effectiveness in diagnosis, therapy, and brain-targeted drug delivery.

Keywords:  mitochondrial communication; mitochondrial dysfunction; mitophagy; neurodegenerative disorders; vesicles

DOI:  https://doi.org/10.1111/ejn.70449