ArticleNature communications2025
Mitochondria transplantation transiently rescues cerebellar neurodegeneration improving mitochondrial function and reducing mitophagy in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 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
- Orally activatable membrane fusion-mitochondria hitchhiking on intestinal macrophages for targeted therapy of bacterial meningitis and neuroinflammation.Bioactive materials · 2027Article
- Mitophagy in cisplatin-induced kidney injury: regulatory mechanisms and therapeutic targets.Annals of medicine · 2026Review
- Mitochondrial remodeling by extracellular vesicles co-delivering functional mitochondria and a mitophagy inducer for neuropathic pain relief.Materials today. Bio · 2026Article
- Convergent Astrocytic Failure in Parkinson's Disease: A System-Level Model of Pathogenesis and Treatment.Molecular neurobiology · 2026Review
- Mitophagy-mediated immune evasion: Shared strategies of pathogens.Redox biology · 2026Review
- Mitochondria as the Hub of Apoptosis: A Comprehensive Insight From Mitochondria to Interactions With Other Organelles.MedComm · 2026Review
- Airway administered artificial mitochondria-enriched nanovesicles for efficient and selective mitochondria transfer to intervene in pulmonary fibrosis.Nature communications · 2026Article
- Targeting Mitochondrial Dysfunction in Microglia: A New Frontier for Treating Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Hierarchical Studies in TRAP2 Mice Demonstrate that Neuronal Activation and Mitochondrial Networks Integration Constitute the Key Mechanism Underlying Painful Syncope.Neuroscience bulletin · 2026Article
- Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats.Journal of orthopaedic translation · 2026Article
- Therapeutic and mechanistic insights on mitochondrial transplantation in kidney disease.Nature reviews. Nephrology · 2026Review
- Mitochondria as convergence hubs for innate immunity pathways.Communications biology · 2026Review
- Reparative "exosome-ark" for mitochondrial transplantation to reprogram macrophages and disrupt pathogenic crosstalk in pulmonary fibrosis.Materials today. Bio · 2026Article
- Article
- Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Drp1-CoQ10-Coa6-ETC axis represents a therapeutic potential for working memory impairment caused by neuronal mitochondrial dysfunction.Translational neurodegeneration · 2026Article
- Therapeutic Potential of Mitochondrial Transplantation with Focus on DBD.International journal of molecular sciences · 2026Review
- Mitochondrial Transplantation in the Eye: A Review and Evaluation of Surgical Approaches.bioRxiv : the preprint server for biology · 2026Article
- Emerging Design Principles at the Forefront of Mitochondrial Transplantation Using Engineering Methodologies: Current Achievements and Future Directions.Chemical biology & drug design · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebellar ataxia is the primary manifestation of cerebellar degenerative diseases, and mitochondrial dysfunction in Purkinje cells (PCs) plays a critical role in disease progression. In this study, we investigated the feasibility of mitochondria transplantation as a potential therapeutic approach to rescue cerebellar neurodegeneration and elucidate the associated mechanisms. We constructed a conditional Drp1 knockout model in PCs (PCKO mice), characterized by progressive ataxia. Drp1 knockout resulted in pervasive and progressive apoptosis of PCs and significant activation of surrounding glial cells. Mitochondrial dysfunction, which triggers mitophagy, is a key pathogenic factor contributing to morphological and functional damage in PCs. Transplanting liver-derived mitochondria into the cerebellum of 1-month-old PCKO mice improved mitochondrial function, reduced mitophagy, delayed apoptosis of PCs, and alleviated cerebellar ataxia for up to 3 weeks. These findings demonstrate that mitochondria transplantation holds promise as a therapeutic approach for cerebellar degenerative diseases.
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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 Socratic graph.