bims-mitrat 2026-09-06 papers

Trends Cell Biol. 2026 Sep 04. pii: S0962-8924(26)00168-6. [Epub ahead of print]

Horizontal mitochondrial transfer: an emerging field in cell biology.

Michael V Berridge, Zuzana Nahacka, Katerina Komrskova, Minghao Zheng, Jiri Neuzil.

The field of horizontal mitochondrial transfer (HMT), also referred to as intercellular mitochondrial transfer, has recently gained momentum due to an increasing number of publications that go well beyond diseases such as cancer. From co-culture experiments to in vivo evidence in mouse cancer models, noncancerous diseases, and normal tissue and organ homeostasis and development, it is becoming increasingly clear that HMT is a fundamental physiological phenomenon broadly relevant to complex organisms. Recent methodological advances, epitomized by ultra-high-resolution microscopy and spatial and single-cell multiomics technologies, allow for research that strongly supports HMT as an emerging area of cell biology.

DOI: https://doi.org/10.1016/j.tcb.2026.08.012

Front Immunol. 2026 ;17 1922061

Mitochondrial transfer: a new perspective on tumor-microenvironment crosstalk driving metastasis.

Yuxuan Duan, Anshu Li, Xun Hu, Zhiyong Xiong, Jian Shi, Keshan Wang.

Tumor metastasis is the leading cause of cancer-related deaths. It depends not only on the intrinsic properties of cancer cells but also on their active shaping of the tumor microenvironment. Recent studies have identified mitochondrial transfer(MT) as a key mechanism underlying this tumor-microenvironment crosstalk. Beyond serving as a simple metabolic rescue pathway, MT functions as an intercellular reprogramming process that promotes metastatic progression. In this Review, we propose that MT acts as a tripartite educator during metastasis by driving three coordinated programs: metabolic licensing, immune rewiring, and stromal remodeling. Metabolic licensing enhances the survival and invasive capacity of cancer cells. Immune rewiring helps tumor cells evade immune surveillance. Stromal remodeling reprograms the tumor microenvironment into a permissive niche that supports tumor establishment. We summarize current evidence supporting each of these three programs and discuss emerging therapeutic strategies aimed at either blocking pathological MT or exploiting it for antitumor intervention.

Keywords: cancer cell plasticity; immune evasion; metastasis; mitochondrial transfer; tumor microenvironment

DOI: https://doi.org/10.3389/fimmu.2026.1922061

Front Immunol. 2026 ;17 1898280

Mitochondria transfer research from cellular mechanisms to immune-inflammatory and translational frontiers: a bibliometric analysis from 2006 to 2026.

Peiwei Su, Wanyu Luo, Chao Zhu, Xudong Zhufu, Xianyi Zhang, Haoxin Wu, Rui Xu, Haijun Zhao.

Background: Mitochondria transfer is an emerging mechanism of intercellular communication involved in mitochondrial homeostasis, metabolic remodeling, immune regulation, inflammatory responses, tumor progression, and mitochondrial transplantation-based therapy. However, the global research landscape and immune-inflammatory frontiers remain unclear.
Methods: Publications on mitochondria transfer published between 1 January 2006 and 8 April 2026, were retrieved from the Web of Science Core Collection and Scopus. After deduplication and manual screening, 851 English-language articles and reviews were analyzed using bibliometrix, CiteSpace, VOSviewer, and Pajek.
Results: The 851 publications included 566 articles and 285 reviews. They received 38,879 citations and an average of 45.69 citations per publication. Annual output increased markedly after 2018 and peaked in 2025. China and the USA were the leading contributors. Journal, co-citation, and keyword analyses showed that mitochondria transfer research has expanded from mitochondrial biology, stem cell-mediated repair, and cellular metabolism toward immune regulation, inflammation, tumor microenvironment remodeling, biomaterials, and translational medicine. Major knowledge bases and emerging hotspots included tunneling nanotubes, extracellular vesicles, mitochondrial transplantation, mitochondrial quality control, metabolic homeostasis, macrophages, T cells, B cells, immune evasion, macrophage polarization, and cGAS/STING-related mechanisms.
Conclusion: Mitochondria transfer has developed into an interdisciplinary field connecting cellular mechanisms, immune-inflammatory regulation, disease microenvironment remodeling, and translational therapy. Future studies should clarify its molecular regulation and context-dependent consequences, particularly in immune cells, inflammatory diseases, tumor immune evasion, and mitochondrial transplantation-based interventions.

Keywords: immune regulation; inflammation; metabolic homeostasis; mitochondria transfer; mitochondria transplantation; mitochondrial quality control

DOI: https://doi.org/10.3389/fimmu.2026.1898280

Methods Mol Biol. 2026 ;3038 477-493

Pronuclear Transfer and Maternal Spindle Transfer in the Mouse.

Ross Stocker, Jeffrey R Mann, John Carroll.

Maternal Spindle Transfer (MST) and Pronuclear Transfer (PNT) are micromanipulation techniques that allow the transfer of the nuclear material from one oocyte or zygote to the cytoplasm of another. The application of these techniques has provided novel insights into nuclear-cytoplasmic interactions necessary for development, as well as fundamental discoveries such as genomic imprinting. Now, after extensive pre-clinical research, PNT and MST are starting to be used clinically for Mitochondrial Donation (also known as mitochondrial replacement therapy) and for patients with a history of repeated IVF failure. Here, we describe the methods for PNT and MST currently used in the mouse model. The techniques are readily adaptable for application to other mammalian species, including humans.

Keywords: Maternal spindle transfer; Mitochondrial disease; Mouse; Oocyte; Pronuclear transfer; Sendai virus; Zygote

DOI: https://doi.org/10.1007/978-1-0716-5292-3_25

Nat Commun. 2026 Aug 05. pii: 9412. [Epub ahead of print]17(1):

Airway administered artificial mitochondria-enriched nanovesicles for efficient and selective mitochondria transfer to intervene in pulmonary fibrosis.

Jinsong Zhang, Siying Fu, Jiawen Wang, Honghui Wu, Zhuoting Li, Ruyi Lin, Hao Sun, Seungho Choe, Yuhuan Kong, Donghang Xu, Jinqiang Wang, Zhen Gu, Jianqing Gao, Tianyuan Zhang.

Mitochondrial transplantation is a promising therapeutic approach involving the transfer of exogenous mitochondria into diseased cells to restore impaired mitochondrial homeostasis. However, its clinical translation is severely limited by the lack of efficient methods for precise and potent mitochondria transfer. Inspired by natural mitochondria-containing vesicles, we develop mesenchymal stem cell-derived biomimetic nanovesicles with high mitochondrial loading capacity and augmented extracellular mitochondrial stability. These nanovesicles exhibit an ability to efficiently and selectively deliver mitochondrial cargo to injured cells, which is potentially ascribed to the specific interaction between very late antigen-5 on the nanovesicle surface and pathologically upregulated fibronectin on injured cells. In a mouse pulmonary fibrosis model, these nanovesicles successfully deliver healthy mitochondria to injured lung epithelial cells through airway administration, resulting in a significant reduction in fibrotic progression. This study introduces a design of mitochondria-enriched biomimetic nanovesicles for effective and targeted mitochondria transfer, offering a nanotechnology-based strategy to advance mitochondrial transplantation therapy.

DOI: https://doi.org/10.1038/s41467-026-76330-9

J Orthop Translat. 2026 Sep;60 101195

ADSC-derived mitochondrial nanovesicles transplantation alleviates capsular fibrosis and inflammation and improves joint mobility in a rat model of adhesive capsulitis.

Yiming Zhu, Zeyu Wang, Ziqi Huo, Dan Zhang, Yang Zhao, Jianhao Xie, Hao Li, Tianyuan Zhao, Pinxue Li, Zhi Wang, Chunyan Jiang, Xu Li.

Background: Adhesive capsulitis (frozen shoulder) is a prevalent condition characterized by shoulder pain and progressive motion loss. Mitochondrial metabolic dysregulation is an underlying driver of chronic inflammation and fibrosis. This study aimed to characterize mitochondrial metabolic abnormalities in patient capsular tissue and evaluate a therapy using adipose-derived stem cell (ADSC) derived mitochondrial nanovesicles transplantation.
Methods: Single-cell RNA sequencing was utilized to analyze the expression of nuclear-encoded genes related to mitochondrial metabolism in fibroblast subpopulations from human adhesive capsulitis capsular tissue. ADSC-derived membranes were extruded together with exogenous mitochondria to generate engineered mitochondrial nanovesicles (AD-Mito-NPs). An inflammatory fibroblast model was employed to assess the uptake of AD-Mito-NPs, along with associated transcriptomic and metabolomic changes, and their effects on apoptosis, inflammation, and extracellular matrix (ECM) remodeling. Finally, AD-Mito-NPs were locally injected into a rat model to evaluate joint movement and histopathology.
Results: AD-Mito-NPs retained intact respiratory function, high fibroblast internalization efficiency, and stable physicochemical properties for up to 7 days. In vitro inflammatory models verified that AD-Mito-NPs reversed IL-1β-triggered mitochondrial injury and strengthened mitochondrial oxidative phosphorylation. Furthermore, AD-Mito-NPs alleviated intracellular reactive oxygen species accumulation and fibroblast apoptosis, mitigated inflammatory responses, and remodeled extracellular matrix homeostasis. In vivo, intra-articular administration of AD-Mito-NPs improved shoulder joint mobility, attenuated capsular thickening and disordered collagen arrangement, and suppressed local inflammation in a rat model of adhesive capsulitis.
Conclusion: Mitochondrial metabolic imbalance is a factor driving capsular fibrosis in adhesive capsulitis. Engineered mitochondrial transplantation offers therapeutic benefits by enhancing mitochondrial energy production, mitigating oxidative stress and inflammation, and restoring ECM balance.
The translational potential of this article: This article identifies mitochondrial metabolic dysregulation as a key driver of adhesive capsulitis-related capsular fibrosis and demonstrates that engineered AD-Mito-NPs are a safe platform for clinical translation. These NPs effectively enhance energy metabolism, reduce inflammation, and improve shoulder mobility in models, providing a promising alternative to existing treatments.

Keywords: Adhesive capsulitis; Adipose-derived stem cell; Capsular fibrosis; Joint inflammation; Mitochondrial dysfunction; Mitochondrial transplantation

DOI: https://doi.org/10.1016/j.jot.2026.101195

Free Radic Biol Med. 2026 Sep 04. pii: S0891-5849(26)01137-8. [Epub ahead of print]

Exercise-Induced Intercellular Mitochondrial Transfer: Redox Signaling as a Candidate Regulatory Mechanism.

Mei Ma, Jinze Tian, Zhe Wang, Ziyi Zhang, Yong Zhang, Hai Bo.

Intercellular mitochondrial transfer has been recognized as an important mechanism for maintaining tissue homeostasis and adapting to stress. Mitochondria can cross cellular boundaries through tunneling nanotubes, extracellular vesicles, and free mitochondrial release. However, the physiological signals coordinating these pathways remain poorly defined. Exercise is a potent inducer of transient redox signaling, generating superoxide and hydrogen peroxide while modulating mitochondrial dynamic remodeling. This review integrates exercise redox biology with redox regulation of transfer machinery characterized in non-exercise models, proposing that exercise-induced redox signaling may function as a candidate regulatory mechanism. The framework emphasizes bidirectional redox coordination, in which oxidant pulses may activate export in donor cells and prepare recipient cells for uptake and antioxidant defense. Exercise-induced mitochondrial transfer has been directly demonstrated in the brain, while observations in skeletal muscle, adipose tissue, and heart remain suggestive but have not been confirmed in exercise models. These findings support a framework in which intercellular mitochondrial transfer contributes to metabolic signaling, antioxidant defense, and distributed quality control across organs. This model represents a working hypothesis requiring direct experimental validation through lineage tracing, tissue-specific mitochondrial reporters, and intravital imaging.

Keywords: exercise; mitochondrial biogenesis; mitochondrial quality control; mitochondrial transfer; redox signaling; tunneling nanotubes

DOI: https://doi.org/10.1016/j.freeradbiomed.2026.09.003