ArticleeLife2023
Transferred mitochondria accumulate reactive oxygen species, promoting proliferation.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondria transfer research from cellular mechanisms to immune-inflammatory and translational frontiers: a bibliometric analysis from 2006 to 2026.Frontiers in immunology · 2026Pooled it
- Intercellular Mitochondrial Transfer in the Nervous System: Roles of Tunneling Nanotubes, Mitochondrial Extracellular Vesicles, and Neuroimmune Bioenergetic Interactions.Molecular neurobiology · 2026Review
- Horizontal mitochondrial transfer and mitochondrial transplantation in skin: protection against UVR-induced ROS damage and enhancement of cell proliferation and wound healing.Journal of translational medicine · 2026Article
- Macrophages transfer functional proteins to their surface during live-cell uptake.Nature chemical biology · 2026Article
- Intercellular mitochondrial transfer and trans-mitophagy in response to protein import dysfunction.The Journal of cell biology · 2026Article
- Article
- Regulation and function of specialized membrane protrusions in intercellular communication.Nature reviews. Molecular cell biology · 2026Review
- Article
- α-Synuclein triggers intercellular nanotubes formation to prevent apoptosis in astroglia by promoting stemness.Cell & bioscience · 2026Article
- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
- Mitochondrial transfer between tumor and immune cells: a nexus of metabolic adaptation and immune dysfunction.Biomarker research · 2026Review
- Mitochondria transfer in glioblastoma.Neuro-oncology · 2026Review
- Engineering exosomes for cancer therapy - Modification technologies and subcellular targeting strategies: A review.International journal of pharmaceutics: X · 2026Review
- Mitophagy in ophthalmic pathologies: Molecular mechanisms and therapeutic implications.Medicine · 2026Review
- Mechanical Force Promotes Mitochondrial Transfer From Macrophages to BMSCs to Enhance Bone Formation.Cell proliferation · 2026Article
- Mitochondrial Transfer in the Tumor Microenvironment.Cancer science · 2026Review
- TCOF1 Regulates Tumor Cell Migration Through p53-Dependent Mitochondrial Homeostasis and F-Actin Dynamics.Current issues in molecular biology · 2026Article
- Intercellular Mitochondrial Transfer: Implications in Cardiovascular Health.Circulation research · 2026Review
- NG2-targeting macrophages inhibit 3D invasion of patient-derived glioblastoma spheroids.bioRxiv : the preprint server for biology · 2026Article
- Monocyte-mediated metabolic rewiring via CD31-CD38 interactions promotes growth and drug-resistance in multiple myeloma.HemaSphere · 2026Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Recent studies reveal that lateral mitochondrial transfer, the movement of mitochondria from one cell to another, can affect cellular and tissue homeostasis. Most of what we know about mitochondrial transfer stems from bulk cell studies and have led to the paradigm that functional transferred mitochondria restore bioenergetics and revitalize cellular functions to recipient cells with damaged or non-functional mitochondrial networks. However, we show that mitochondrial transfer also occurs between cells with functioning endogenous mitochondrial networks, but the mechanisms underlying how transferred mitochondria can promote such sustained behavioral reprogramming remain unclear. We report that unexpectedly, transferred macrophage mitochondria are dysfunctional and accumulate reactive oxygen species in recipient cancer cells. We further discovered that reactive oxygen species accumulation activates ERK signaling, promoting cancer cell proliferation. Pro-tumorigenic macrophages exhibit fragmented mitochondrial networks, leading to higher rates of mitochondrial transfer to cancer cells. Finally, we observe that macrophage mitochondrial transfer promotes tumor cell proliferation in vivo. Collectively these results indicate that transferred macrophage mitochondria activate downstream signaling pathways in a ROS-dependent manner in cancer cells, and provide a model of how sustained behavioral reprogramming can be mediated by a relatively small amount of transferred mitochondria in vitro and in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.