Evidence map›Paper›PMID 29367651›Full record

ArticleScientific reports2018

Embryonic Surface Ectoderm-specific Mitofusin 2 Conditional Knockout Induces Congenital Cataracts in Mice.

Jiangyue Zhao, Xinwei Wu, Danhong Wu, Yinhui Yu, Yibo Yu, Yao Wang, Qiuli Fu, Jinsong Zhang, Ke Yao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Polyunsaturated fatty acid metabolism in the retinal pigment epithelium and its association with outer retinal disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts.Investigative ophthalmology & visual science · 2021
    Article
  7. Review
  8. Article
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

9 authors at 5 institutions in 1 country.

Jiangyue ZhaoThe Department of ophthalmology, Eye center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, 310009, China.
Xinwei WuThe Department of ophthalmology of the 4th Affiliated Hospital, China Medical University, Shenyang, 110005, China.
Danhong WuDepartment of Neurology, Shanghai fifth People's Hospital, Fudan University, Shanghai, 200240, China.
Yinhui YuThe Department of ophthalmology, Eye center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, 310009, China.
Yibo YuThe Department of ophthalmology, Eye center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, 310009, China.
Yao WangThe Department of ophthalmology, Eye center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, 310009, China.
Qiuli FuThe Department of ophthalmology, Eye center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, 310009, China.
Jinsong ZhangThe Department of ophthalmology of the 4th Affiliated Hospital, China Medical University, Shenyang, 110005, China.
Ke YaoThe Department of ophthalmology, Eye center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, 310009, China. xlren@zju.edu.cn.
Zhejiang University · CNChina Medical University · CNWenzhou Medical University · CNAffiliated Eye Hospital of Wenzhou Medical College · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inherited mitochondrial mutations can result in mitochondrial dysfunction or stochastic oxidative damage. Cumulative mitochondrial damage is an important factor in age-related disorders, such as cataracts and macular degeneration. Mfn2 mediates the fusion of mitochondria and contribute to the dynamic balance between fusion and fission that determines mitochondria morphology. We report here that conditional loss of Mfn2 function in the head surface ectoderm leads to a range of congenital eye defects, including small, opacified lens and small eyeball in the most severe phenotypes. The Le-Cre transgenic mouse line and Mfn2 flox mouse line were used in this study to generate Mfn2 conditional knockout mice. Our study revealed Mfn2 gene function in lens development and addressed the relationship between the mitochondria and lens transparency. Conditional loss of Mfn2 affected lens epithelium cell proliferation, apoptosis and ultrastructure of mitochondria. We conclude that proper development of the lens and lens transparency depend on normal Mfn2 gene function.

Indexed as

AnimalsCataractDisease Models, AnimalGene Knockdown TechniquesGTP PhosphohydrolasesLens, CrystallineMice, KnockoutGTP PhosphohydrolasesMfn2 protein, mouse

Identifiers

PMID29367651
PMCPMC5784114
OpenAlexW2801139037

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.