bims-mitrat 2026-07-26 papers

Wound Repair Regen. 2026 Jul-Aug;34(4):34(4): e70192

Mitochondrial Transplantation Increases Dermal Fibroblast Proliferation and Accelerates Acute Wound Closure.

Ikkei Takashimizu, Miho Noguchi, Shunsuke Yuzuriha.

The detrimental effects of dysfunctional mitochondria on cells and tissues have been shown to improve by healthy mitochondria transplantation. However, the feasibility of intercellular mitochondrial transfer for wound healing remains uncertain. This study examined whether healthy mitochondria transplantation promoted the healing of acute wounds. Isolated mitochondria derived from primary cultured normal human dermal fibroblasts were administered to primary cells of the same lineage, with confirmed cell uptake. Wound closure rate in in vitro scratch wound healing assays increased in a dose-dependent manner and was attenuated by treatment with the mitochondrial function inhibitor antimycin A. Gene expression analysis revealed significant increases in the cell proliferation markers MKI67 and PCNA, although no consistent changes in migration-related genes were observed. Cell proliferation rate increased to a maximum average of 1.4-fold after isolated mitochondrial administration, which was attenuated by antimycin A treatment. To verify the in vivo effects of isolated mitochondrial transplantation, mitochondria were obtained from mouse livers, and wound closure rate was analysed using a mouse wound healing model. The number of days to wound closure was significantly shortened in a dose-dependent manner, and this gain was attenuated by antimycin A. Our findings demonstrate that mitochondrial transplantation accelerates acute wound closure and enhances fibroblast proliferative activity. The observed increase in cell proliferation may contribute, at least in part, to the beneficial effects of mitochondrial transplantation on wound healing. These findings provide insight into the therapeutic potential of mitochondrial transplantation as a novel strategy for wound repair.

Keywords: cell proliferation; isolated mitochondria; mitochondrial transplantation; wound healing

DOI: https://doi.org/10.1111/wrr.70192

Front Oncol. 2026 ;16 1872429

Mitochondrial transfer in cancer: a global bibliometric analysis.

Yang Lu, Liangkai Zhu, Yang Xu, Sihong Ye, Yana Wang, Baicheng Ni, Ming Zheng, Wanglong Chen.

Background: Mitochondrial transfer is increasingly recognized as a biologically meaningful mode of intercellular communication in cancer. Its involvement in tumor metabolism, microenvironmental interaction, therapeutic adaptation, and immune regulation has driven rapid growth of the field. However, bibliometric assessment of its global research landscape has remained lacking.
Methods: A bibliometric analysis was performed using literature retrieved from the Web of Science Core Collection, Scopus, and PubMed. English-language articles and reviews published between 1981 and 2025 were included. Bibliometrix, CiteSpace, and VOSviewer were used to evaluate publication trends, countries, institutions, authors, journals, citation networks, and keyword co-occurrence patterns.
Results: A total of 184 publications were identified. Annual output increased sharply after 2016 and reached a peak of 48 papers in 2025. The literature was distributed across 117 journals, with 16 core journals identified according to Bradford's law. The principal citation pathway extended from molecular, biology, and immunology journals to molecular, biology, and genetics journals, indicating a knowledge base rooted mainly in molecular and cellular mechanisms. China ranked first in publication output, followed by the United States. INSERM, Changhua Christian Hospital, and Sichuan University were the leading institutions. Neuzil J was the most productive author, whereas Berridge MV had the highest citation impact. The most cited reference was "Mitochondrial transfer between cells can rescue aerobic respiration". Keyword evolution indicated a thematic shift from earlier emphases on mesenchymal stem cells, tunneling nanotubes, and mitochondrial transfer toward mitochondrial transplantation and the tumor microenvironment.
Conclusions: Research on mitochondrial transfer in cancer has progressed from early mechanistic observation to a rapidly expanding field with increasing translational relevance. Current hotspots center on mitochondrial transplantation, tumor-microenvironment interactions, metabolic adaptation, and therapy-related biological processes such as chemoresistance and apoptosis. Further progress will require stronger causal validation, methodological standardization, and closer integration with clinically relevant models.

Keywords: bibliometric analysis; cancer therapy; mitochondrial transfers; mitochondrial transplantation; tumor microenvironment

DOI: https://doi.org/10.3389/fonc.2026.1872429

Trends Mol Med. 2026 Jul 23. pii: S1471-4914(26)00172-3. [Epub ahead of print]

Mitochondrial transfer: quality dictates immune-metabolic fate.

Kai Liu, Quazi T H Shubhra, Hui Zhang.

Horizontal mitochondrial transfer (HMT) outcomes are shaped by donor fitness and transfer context. We propose a post-transfer quality checkpoint that integrates membrane potential, oxidative damage, mitophagy, fusion, and fission to determine the recipient-cell's response. Depending on donor quality and recipient thresholds, HMT may drive bioenergetic restoration, inflammation, or tumor immune escape. This framework extends route-centered accounts of HMT toward a testable, quality-governed model for therapeutic intervention.

Keywords: immune-metabolic fate; mitochondrial quality; mitochondrial transfer; quality checkpoint

DOI: https://doi.org/10.1016/j.molmed.2026.07.002

Stem Cell Rev Rep. 2026 Jul 18.

Mitochondrial Communication Networks in the Bone Microenvironment: From the Maintenance of Homeostasis to Translational Interventions for Bone Diseases.

Wentao Wang, Kun Wang, Wenjing Wang, Xuan Mu, Zhiquan Cheng, Guangzhi Zhang, Xuewen Kang, Yonggang Wang.

Intercellular mitochondrial transfer has recently emerged as an important concept in bone biology, providing a new framework for understanding immune-metabolic cross-talk within the bone microenvironment. This microenvironment is a dynamic system that is both metabolically active and immunologically complex, and its homeostasis relies on finely tuned communication among multiple cellular populations. Increasing evidence suggests that mitochondrial transfer is a key mechanism integrating these diverse signaling networks. In this review, we systematically summarize recent advances in mitochondrial transfer among osteolineage cells, immune cells, and vascular-associated cells, and we further discuss its multiple roles in bone remodeling, tissue repair, and the pathogenesis of osseous diseases. At the mechanistic level, special emphasis is placed on the Mitochondrial Rho GTPase 1 (MIRO1)-mediated mitochondrial transport pathway, through which mitochondria are transferred from osteolineage cells to myeloid cells, thereby driving metabolic reprogramming and modulating susceptibility to ferroptosis, ultimately helping to suppress excessive osteoclastogenesis. From a pathological perspective, dysregulated mitochondrial transfer is increasingly recognized as a common feature across a range of skeletal disorders. In glucocorticoid-induced osteoporosis (GIOP), impairment of MIRO1-dependent mitochondrial transport promotes ferroptosis resistance in osteoclast precursors. In osteoarthritis, aberrant mitochondria accelerate cartilage degeneration by disrupting coenzyme A (CoA) metabolism through Nudix Hydrolase 8 (NUDT8) and subsequently activating the cGAS-STING signaling pathway. In bone metastasis, inflammatory signals triggered by mitochondrial deoxyribonucleic acid (mtDNA) release exhibit both pro-tumorigenic and anti-tumorigenic regulatory effects. Based on these mechanisms, this manuscript also critically evaluates the translational potential of several therapeutic strategies, including mesenchymal stem cell-derived mitochondrial transplantation, nanocarrier delivery systems, and the modulation of tunneling nanotubes. Overall, targeting intercellular mitochondrial transport may offer new therapeutic opportunities for metabolic intervention and immunomodulation in bone diseases.

Keywords: Bone microenvironment; Ferroptosis; Intercellular mitochondrial transfer; Metabolic reprogramming; Mitochondrial transplantation; Osteoimmunology; Tunneling nanotubes

DOI: https://doi.org/10.1007/s12015-026-11190-w

Stem Cell Res Ther. 2026 Jul 20.

Miro1-mediated mitochondrial transfer boosts stem cell therapy for muscle atrophy via restoring mitochondrial homeostasis.

Fangling Zhao, Jingxin Fu, Linli Gao, Mengting Zhou, Yuhui Xia, Zexian Zhao, MengNa Yang, Jiahui He, Wei Zhu, Mengxiong Pan, Kaiming Liu.

Mitochondrial dysfunction underlies the major defect in muscle atrophy (characterized by the loss of skeletal muscle mass and function). Mesenchymal stem cells (MSCs), which can mediate mitochondrial transfer (MT) via tunneling nanotubes (TNTs), have been shown to exert therapeutic effects, yet the underlying mechanism remains unclear. Mitochondrial Rho GTPase 1 (Miro1) is crucial for regulating mitochondrial homeostasis; in this study, we aimed to investigate the roles of Miro1 and Milton in MSC-based therapy for muscle atrophy. Dexamethasone (DEX)-induced C2C12 cells and chronically aged mice were used as in vitro cellular and in vivo muscle atrophy models, respectively. In vitro experiments demonstrated that overexpression of Milton alone failed to enhance MT in DEX-induced C2C12 cells. Although Milton could promote the formation of TNTs, it was unable to drive mitochondrial movement along microtubules in the absence of Miro1.In contrast, Miro1 knockdown (MSCmiro1Lo) significantly reduced MT in vivo, while Miro1 overexpression (MSCmiro1Hi) improved mitochondrial morphology, increased muscle fiber count and cross-sectional area, upregulated the expression of type I/III collagen, and downregulated the expression of Atrogin1 and MURF1. Additionally, Miro1 overexpression ameliorated functional outcomes such as grip strength, running distance, and physical activity, and elevated the levels of proteins related to mitochondrial fusion, mitophagy, and biogenesis in damaged muscle cells. These findings indicate that Miro1 is a critical driver of MT, and Miro1-enhanced MT confers substantial in vivo therapeutic benefits. This study provides robust evidence supporting Miro1 as a potential target for the treatment of muscle atrophy-related disorders.

Keywords: Miro1; Mitochondrial homeostasis; Mitochondrial transfer; Muscle atrophy; Stem cells

DOI: https://doi.org/10.1186/s13287-026-05191-2