Evidence map›Paper›PMID 41353207›Full record

ArticleNature communications2025

CRISPR-free RNA base editing mediated PTC-readthrough restores hearing in mice with Otof nonsense mutation.

Hanxiao Sun, Qi Teng, Wenqing Liu, Rui Guo, Menghua Li, Wei Xiong, Qiang Huang, Qianru Yu, Nan Luo, Yang Li and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. The impact of psuedouridine modification on human tRNA.Biochemical Society transactions · 2026
    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

15 authors.

Hanxiao Sun *The National Key Laboratory of Gene Function Studies and Manipulation, School of Life Sciences, Peking University, Beijing, China.
Qi Teng *Department of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Wenqing Liu *School of Life Sciences, Tsinghua University, Beijing, China.
Rui Guo *Department of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0002-6708-526X
Menghua Li *Department of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Wei XiongDepartment of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Qiang HuangThe National Key Laboratory of Gene Function Studies and Manipulation, School of Life Sciences, Peking University, Beijing, China.
Qianru YuDepartment of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Nan LuoThe National Key Laboratory of Gene Function Studies and Manipulation, School of Life Sciences, Peking University, Beijing, China.
Yang LiDepartment of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0003-2626-6088
Jinghui SongThe National Key Laboratory of Gene Function Studies and Manipulation, School of Life Sciences, Peking University, Beijing, China.ORCID http://orcid.org/0000-0003-2225-7977
Shusheng GongDepartment of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Xi ShiAcademician Workstation of Hainan University (Sanya), School of Pharmaceutical Sciences, Hainan University, Haikou, Hainan, China. shixi2023@hainanu.edu.cn.
Chengqi YiThe National Key Laboratory of Gene Function Studies and Manipulation, School of Life Sciences, Peking University, Beijing, China. chengqi.yi@pku.edu.cn.ORCID http://orcid.org/0000-0003-2540-9729
Ke LiuDepartment of Otolaryngology Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China. liuke@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-0505-920X

Funding

National Natural Science Foundation of China (National Science Foundation of China) no. 81770997National Natural Science Foundation of China (National Science Foundation of China) no. 82460223
6 · The paper itself

Abstract

The gene therapy achieved by AAV-mediated otoferlin-overexpression is an effective therapeutic strategy for congenital deafness. However, achieving its physiological and endogenous patterns of expression remains challenging. Here, we generate the homologous mutation Otof c.1315 C > T (p.R439*), equivalent to OTOF c.1273 C > T (p.R425*) found in humans with profound deafness, to create a nonsense mutation-induced deaf mouse model. We then deliver the 'RESTART v3' system, which is a CRISPR-free RNA base editor for nonsense mutation suppression, into the cochlea of the mice. We achieve physiological otoferlin expression, and the edited premature termination codon is reverse-mutated to the original amino acid. We observe significant hearing restoration and enhancement of the behavioral auditory startle reflex. Thus, our study presents a successful RNA editing strategy to significantly restore hereditary deafness in mice carrying the specific Otof nonsense mutation, which holds great promise for future clinical translation.

Indexed as

Codon, NonsenseDeafnessGenetic TherapyHearingMembrane ProteinsRNA EditingAnimalsCochleaCRISPR-Cas SystemsDisease Models, AnimalFemaleGene EditingHumansMaleMiceMice, Inbred C57BLCodon, NonsenseMembrane Proteins

Identifiers

PMID41353207
PMCPMC12796263

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.