Evidence map›Paper›PMID 33348803›Full record

ReviewInternational journal of molecular sciences2020

Anti-Kir4.1 Antibodies in Multiple Sclerosis: Specificity and Pathogenicity.

Michie Imamura, Osamu Higuchi, Yasuhiro Maeda, Akihiro Mukaino, Mitsuharu Ueda, Hidenori Matsuo, Shunya Nakane

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 31% of its field
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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  2. Review
  3. Review
  4. Alcohol Consumption and Autoimmune Diseases.International journal of molecular sciences · 2025
    Review
  5. Article
  6. 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

7 authors at 3 institutions in 1 country.

Michie ImamuraDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8555, Japan.
Osamu HiguchiDepartment of Clinical Research, National Hospital Organization Nagasaki Kawatana Medical Center, Nagasaki 859-3615, Japan.
Yasuhiro MaedaDepartment of Clinical Research, National Hospital Organization Nagasaki Kawatana Medical Center, Nagasaki 859-3615, Japan.
Akihiro MukainoDepartment of Molecular Neurology and Therapeutics, Kumamoto University Hospital, Kumamoto 860-8556, Japan.ORCID 0000-0001-7486-0597
Mitsuharu UedaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8555, Japan.
Hidenori MatsuoDepartment of Neurology, National Hospital Organization Nagasaki Kawatana Medical Center, Nagasaki 859-3615, Japan.
Shunya NakaneDepartment of Molecular Neurology and Therapeutics, Kumamoto University Hospital, Kumamoto 860-8556, Japan.ORCID 0000-0003-1958-095X
Nagasaki Kawatana Medical Center · JPKumamoto University · JPKumamoto University Hospital · JP

Funding

MEXT/JSPS KAKENHI 19H03549
6 · The paper itself

Abstract

The glial cells in the central nervous system express diverse inward rectifying potassium channels (Kir). They express multiple Kir channel subtypes that are likely to have distinct functional roles related to their differences in conductance, and sensitivity to intracellular and extracellular factors. Dysfunction in a major astrocyte potassium channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurological diseases. The autoimmune effects on the potassium channel have not yet been fully described in the literature. However, several research groups have reported that the potassium channels are an immune target in patients with various neurological disorders. In 2012, Srivastava et al. reported about Kir4.1, a new immune target for autoantibodies in patients with multiple sclerosis (MS). Follow-up studies have been conducted by several research groups, but no clear conclusion has been reached. Most follow-up studies, including ours, have reported that the prevalence of Kir4.1-seropositive patients with MS was lower than that in the initial study. Therefore, we extensively review studies on the method of antibody testing, seroprevalence of MS, and other neurological diseases in patients with MS. Finally, based on the role of Kir4.1 in MS, we consider whether it could be an immune target in this disease.

Indexed as

AnimalsAutoantibodiesHumansKcnj10 ChannelMultiple SclerosisPotassium Channels, Inwardly RectifyingAutoantibodiesKcnj10 ChannelPotassium Channels, Inwardly RectifyingautoantibodyKir4.1multiple sclerosisneurological diseasepotassium channel

Identifiers

PMID33348803
PMCPMC7765826
OpenAlexW3113156900

What OpenQuestion 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 OpenQuestion graph.