Evidence map›Paper›PMID 39901658›Full record

ArticleAnnals of clinical and translational neurology2025

Blood exosome connexins and small RNAs related to demyelinating disease activity.

Guzailiayi Maimaitijiang, Jun-Ichi Kira, Yuri Nakamura, Mitsuru Watanabe, Ezgi Ozdemir Takase, Satoshi Nagata, Ayako Sakoda, Xu Zhang, Katsuhisa Masaki, Ryo Yamasaki and 3 more

Abstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

13 authors.

Guzailiayi Maimaitijiang *Translational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Jun-Ichi Kira *Translational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.ORCID 0000-0001-5307-2671
Yuri NakamuraTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Mitsuru WatanabeDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID 0000-0003-0831-623X
Ezgi Ozdemir TakaseDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Satoshi NagataDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Ayako SakodaTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Xu ZhangTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Katsuhisa MasakiDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Ryo YamasakiDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Noriko IsobeDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Hiroo YamaguchiDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tomohiro ImamuraTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.

Funding

Japan Agency for Medical Research and Development (AMED) 21ek0109547h0001Japan Agency for Medical Research and Development (AMED) 22ek0109547h0002Japan Agency for Medical Research and Development (AMED) 23ek0109547h0003Japan Agency for Medical Research and Development (AMED) 23ek0109626h0001Japan Agency for Medical Research and Development (AMED) 23ek010962h0002Japan Agency for Medical Research and Development (AMED) 24wm0625504s01001Japan Society for the Promotion of Science KAKENHI JP22H02985Japan Society for the Promotion of Science KAKENHI JP22K07351Japan Society for the Promotion of Science KAKENHI JP23K14761Japan Society for the Promotion of Science KAKENHI JP23K18266Japan Society for the Promotion of Science KAKENHI JP23K24246Japan Society for the Promotion of Science KAKENHI JP24K02371Japan Society for the Promotion of Science KAKENHI JP24K10666Japan Society for the Promotion of Science KAKENHI JP24K18710
6 · The paper itself

Abstract

objectivesTo assess blood exosome (Ex)-connexin (Cx)43 (encoded by GJA1) and its truncated isoforms in multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), which show distinct alterations in astroglial Cx43.

methodsSerum Exs from 48 patients with MS (34 relapsing-remitting, 14 secondary-progressive), 35 with NMOSD, 20 with other inflammatory neurologic diseases (OIND), and 17 healthy controls (HC) were subjected to quantitative Western blotting for Cx43, single-molecule array for neurofilament-L, and quantitative polymerase chain reaction for non-coding RNAs detected by RNA sequencing. Sera from control and astroglia-specific Cx43 inducible conditional knockout (Cx43-icKO) mice with experimental autoimmune encephalomyelitis (EAE) were also tested.

resultsEx-GJA1-29k was markedly higher in MS than in NMOSD, OIND, and HC; it successively increased at relapse, remission, and secondary progression, and positively correlated with disability scores. Ex-hsa-miR-133b and other hsa-miRs that bind to full-length Cx43 were significantly lower in secondary-progressive MS than in HC, and Ex-hsa-miR-133b was negatively correlated with disability scores. Ex-GJA1-11k expression was lower in NMOSD at relapse than in HC and OIND, and was negatively correlated with disability score worsening and Ex-neurofilament-L levels. NMOSD at relapse had significantly higher expression of small nucleolar RNA (SNORD37, SNORD95, and SNORD97) than HC, and SNORD37 and SNORD95 showed strong negative correlations with disability scores. Control mice showed increased Ex-GJA1-43k and -29k during EAE; this effect was markedly reduced in Cx43-icKO mice with attenuated EAE.

interpretationBlood Ex-Cx43-truncated isoforms and small non-coding RNAs, which partially come from brain astroglia, are distinctly dysregulated in MS and NMSOD.

Indexed as

Connexin 43ExosomesMicroRNAsMultiple SclerosisNeuromyelitis OpticaAdultAnimalsEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansMaleMiceMice, KnockoutMiddle AgedConnexin 43GJA1 protein, humanMicroRNAs

Identifiers

PMID39901658
PMCPMC11920735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.