ArticleFrontiers in immunology2026
Mitochondrial transplantation ameliorates experimental autoimmune encephalomyelitis by modulating the Th17/Treg balance and restoring metabolic homeostasis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Mitochondrial dysfunction has been increasingly implicated in the pathogenesis of multiple sclerosis (MS), contributing to oxidative stress, immune dysregulation, and neurodegeneration. Current therapies primarily target inflammation but do not adequately address mitochondrial impairment or progressive tissue damage. This study aimed to evaluate the therapeutic potential of mitochondrial transplantation in experimental autoimmune encephalomyelitis (EAE), a murine model of MS, by investigating its effects on immune modulation, mitochondrial function, and tissue integrity. Methods: EAE was induced in mice using myelin oligodendrocyte glycoprotein. Isolated mitochondria were administered intravenously, and clinical progression, spinal cord histology, immune cell populations, mitochondrial activity, fibrosis, and gut microbiota composition were assessed. Additionally, human peripheral blood mononuclear cells (PBMCs) from MS patients were co-cultured with mitochondria to examine ATP production, reactive oxygen species levels, and T cell differentiation. Results: Mitochondrial transplantation significantly reduced EAE severity, spinal cord inflammation, demyelination, and fibrosis. Treated mice showed increased regulatory T (Treg) cells, reduced T helper 17 (Th17) cells, improved mitochondrial biogenesis, and decreased oxidative stress. Gut microbiome analysis revealed beneficial compositional changes. In human PBMCs, mitochondrial transfer enhanced ATP synthesis, suppressed mitochondrial ROS, and promoted Treg differentiation while inhibiting pro-inflammatory cytokines. Discussion: Our findings suggest that mitochondrial transplantation restores mitochondrial function, rebalances immune responses, and mitigates neuroinflammation and fibrosis in EAE. This approach offers a novel therapeutic strategy for MS by addressing both metabolic and immunological drivers of disease progression.
Indexed as
Identifiers
What OpenQuestion holds
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.