Evidence map›Paper›PMID 39191959›Full record

ArticleTranslational stroke research2025

RNF213 Mutation Associated with the Progression from Middle Cerebral Artery Steno-Occlusive Disease to Moyamoya Disease.

Tomoki Sasagasako, Yohei Mineharu, Takeshi Funaki, Yasutaka Fushimi, Hideo Chihara, Silsu Park, Kota Nakajima, Yasuzumi Matsui, Masakazu Okawa, Takayuki Kikuchi and 1 more

Abstract read
In one paragraph

Article in Translational stroke research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. An Overview of Genetics of Moyamoya: BeyondInternational journal of molecular sciences · 2026
    Review
  2. Long-term outcomes in the pre-moyamoya stage ofThe Lancet regional health. Western Pacific · 2026
    Article
  3. Peripheral bloodStroke and vascular neurology · 2025
    Article
  4. 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

11 authors.

Tomoki SasagasakoDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yohei MineharuDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan. mineharu@kuhp.kyoto-u.ac.jp.
Takeshi FunakiDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan. tfunaki@kuhp.kyoto-u.ac.jp.
Yasutaka FushimiDepartment of Diagnostic Imaging and Nuclear Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hideo ChiharaDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Silsu ParkDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kota NakajimaDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yasuzumi MatsuiDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masakazu OkawaDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takayuki KikuchiDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yoshiki ArakawaDepartment of Neurosurgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Funding

Japan Agency for Medical Research and Development JP21bm0804032h0001, JP22bm0804032h0002, JP23bm0804032h0003Ministry of Education, Culture, Sports, Science and Technology of Japan KAKENHI 17H06397, 19H03770
6 · The paper itself

Abstract

Middle cerebral artery steno-occlusive disease (MCAD) has been recognized as a different clinical entity from moyamoya disease (MMD). Although MCAD can progress to MMD, the extent to which patients actually progress and the risk factors for this progression have not been fully elucidated. We retrospectively reviewed patients with MCAD who underwent RNF213 genotyping. Demographic features, RNF213 p.R4810K mutation, medical history, and longitudinal changes in angiography were analyzed. Sixty patients with 81 affected hemispheres were enrolled. During the follow-up period, 17 patients developed MMD, and the RNF213 p.R4810K mutation was the only factor significantly associated with progression to MMD (odds ratio, 16.1; 95% CI, 2.13-731; P = 0.001). The log-rank test demonstrated that patients with the mutation had a higher risk of progression to MMD (P = 0.007), stenosis progression (P = 0.010), and symptomatic cerebral infarction or hemorrhage (P = 0.026). In Cox regression analysis the p.R4810K mutation remained a significant factor after adjusting for age group (childhood or adult onset) at diagnosis (hazard ratio, 8.42; 95% CI, 1.10-64.4). Hemisphere-based analysis also showed that the mutation was associated with a higher risk of progression to the MMD hemisphere (P = 0.002), stenosis progression (P = 0.005), and cerebral infarction or hemorrhage (P = 0.012). The RNF213 p.R4810K mutation was identified as a risk factor for progression from MCAD to MMD. Genotyping for this mutation may contribute to risk stratification in MCAD.

Indexed as

Adenosine TriphosphatasesInfarction, Middle Cerebral ArteryMoyamoya DiseaseMutationUbiquitin-Protein LigasesAdolescentAdultChildDisease ProgressionFemaleHumansMaleMiddle AgedRetrospective StudiesYoung AdultAdenosine TriphosphatasesRNF213 protein, humanUbiquitin-Protein LigasesAtherosclerosisDisease progressionMiddle cerebral artery occlusionMoyamoya diseaseRNF213

Identifiers

PMID39191959
PMCPMC12202527

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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 OpenQuestion graph.