Evidence map›Paper›PMID 29750298›Full record

ArticleInternational journal of molecular medicine2018

Role of Smad3 signaling in the epithelial‑mesenchymal transition of the lens epithelium following injury.

Fanlan Meng, Jun Li, Xiao Yang, Xiaoyong Yuan, Xin Tang

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  5. Anterior Capsular Contraction Syndrome in Cataract Surgery: A Review of Challenges and Solutions.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Fanlan MengClinical College of Ophthalmology, Tianjin Medical University, Tianjin 300020, P.R. China.
Jun LiClinical College of Ophthalmology, Tianjin Medical University, Tianjin 300020, P.R. China.
Xiao YangThe State Key Laboratory of Proteomics, Genetics Laboratory of Development and Disease, Institute of Biotechnology, AMMS, Beijing 100071, P.R. China.
Xiaoyong YuanClinical College of Ophthalmology, Tianjin Medical University, Tianjin 300020, P.R. China.
Xin TangClinical College of Ophthalmology, Tianjin Medical University, Tianjin 300020, P.R. China.
Tianjin Medical University · CNState Key Laboratory of Proteomics

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor‑β (TGF‑β) is important in the development of posterior capsule opacification (PCO), and inhibition of the TGF‑β pathway may represent a novel method of treating PCO. Drosophila protein, mothers against decapentaplegic homolog 3 (Smad3) is a phosphorylated receptor‑activated Smad required for the transmission of TGF‑β signals. Smad3 knockout (KO) disturbs the activation of TGF‑β signaling, thus inhibiting the onset of PCO. In the present study, lens epithelial cell (LEC) damage induced by extracapsular cataract extraction was simulated by puncture of the anterior capsule using a 26‑gauge hypodermic needle. The effect of Smad3 in the trauma‑induced epithelial‑mesenchymal transition (EMT) of the lens epithelium in Smad3‑KO and wild‑type (WT) mice was then observed. The expression levels of EMT markers and extracellular matrix components were measured in the two groups by reverse transcription‑quantitative polymerase chain reaction analysis, western blot analysis and immunofluorescence staining. Apoptosis was also detected in the punctured anterior capsule. The Smad3‑KO mice exhibited lower expression levels of α‑smooth muscle actin, lumican, osteopontin, fibronectin and collagen, compared with the WT mice. Additionally, the Smad3‑KO mice exhibited a higher percentage of apoptotic cells than the WT mice. Smad3 signaling was associated with the induction of trauma‑induced EMT, and Smad3 KO interfered with TGF‑β signaling pathway activation, but did not completely inhibit the trauma‑induced EMT in LECs. Therefore, Smad3 may be a target in the treatment of PCO and other fibrosis‑related diseases.

Indexed as

Epithelial-Mesenchymal TransitionSignal TransductionAnimalsApoptosisEpithelial CellsFemaleFibrosisGene DeletionLens, CrystallineMaleMiceMice, Inbred C57BLMice, KnockoutSmad3 ProteinSmad3 ProteinSmad3 protein, mouse

Identifiers

PMID29750298
PMCPMC6034923
OpenAlexW2800467601

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.