Evidence map›Paper›PMID 40274784›Full record

ArticleNature communications2025

TGF-β1-induced m6A modifications accelerate onset of nuclear cataract in high myopia by modulating the PCP pathway.

Ling Wei, Yu Du, Shunxiang Gao, Dan Li, Keke Zhang, Wenwen He, Yi Lu, Xiangjia Zhu

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
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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

8 authors.

Ling Wei *Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-9086-4368
Yu Du *Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Shunxiang Gao *Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0001-5267-6289
Dan LiDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-8841-8991
Keke ZhangDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Wenwen HeDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Yi LuDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Xiangjia ZhuDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China. zhuxiangjia1982@126.com.ORCID http://orcid.org/0000-0001-6131-9582

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82122017, 82271069, 81870642, 81970780, 81470613 and 81670835
6 · The paper itself

Abstract

High myopia is an important cause of visual impairment worldwide, characterized by early-onset nuclear cataracts, whose underlying mechanisms remain largely unexplained. Here, we identify conspicuously polarized and compacted lens fiber alignment, along with a simultaneous rise in N6-methyladenosine (m6A) modifications in patients with highly myopic cataracts (HMC), which is confirmed to be induced by elevated transforming growth factor-β1 (TGF-β1) in lens. Mechanistically, methyltransferase METTL3 and m6A reader insulin-like growth factor 2 mRNA binding protein 3 synergistically enhance planar cell polarity (PCP) signaling by affecting mRNA stability of dishevelled 2. This, in turn, alters proliferation, migration, and polarity formation of human lens epithelial cells. Moreover, Mettl3 conditional knockdown in mice leads to disrupted lens fiber arrangement and alleviates TGF-β1-induced increase in lens nuclear density. Collectively, these findings highlight the significance of m6A-modified PCP pathway in regulating postnatal lens fiber organization, which may hold great promise as a therapeutic target for HMC.

Indexed as

AdenosineCataractCell PolarityMyopiaTransforming Growth Factor beta1Adaptor Proteins, Signal TransducingAnimalsCell MovementCell ProliferationEpithelial CellsFemaleHumansLens, CrystallineMaleMethyltransferasesMiceAdaptor Proteins, Signal TransducingAdenosineMethyltransferasesMETTL3 protein, humanN-methyladenosineRNA-Binding ProteinsTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID40274784
PMCPMC12022316

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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.