Evidence map›Paper›PMID 41995755›Full record

ReviewCellular and molecular neurobiology2026

Mitochondrial-Immune Dysfunction in MS: Therapeutic Potential of EV-Mediated Transfer.

Parsa Navazi, Mohammad Fereidouni, Nafiseh Erfanian

Abstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Parsa NavaziStudent Research Committee, Birjand University of Medical Sciences, Birjand, Iran.
Mohammad FereidouniCellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Nafiseh ErfanianCellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran. nafiseherfanian@gmail.com.ORCID http://orcid.org/0000-0002-4348-272X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system. In this disease, mitochondrial dysfunction contributes to neurodegeneration, axonal loss, and progressive disability. Extracellular vesicle (EV)-mediated mitochondrial transfer has emerged as a promising cell-free strategy to restore mitochondrial homeostasis and modulate immune responses within the CNS. Preclinical studies, particularly in experimental autoimmune encephalomyelitis models, demonstrate that EV-based delivery of mitochondrial cargo improves cellular bioenergetics. In parallel, this approach reduces oxidative stress and neuroinflammation while supporting remyelination and neuroprotection. This review summarizes the mechanistic rationale, current preclinical evidence, and future translational perspectives of EV-mediated mitochondrial therapy in MS.

Indexed as

Extracellular VesiclesMitochondriaMultiple SclerosisAnimalsHumansExtracellular vesiclesMitochondriaMultiple sclerosisNeurodegenerationNeuroinflammation

Identifiers

PMID41995755
PMCPMC13216381

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.