Evidence map›Paper›PMID 23426374›Full record

ArticleThe Journal of biological chemistry2013

Sma- and Mad-related protein 7 (Smad7) is required for embryonic eye development in the mouse.

Rui Zhang, Heng Huang, Peijuan Cao, Zhenzhen Wang, Yan Chen, Yi Pan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Elevated TGFβ signaling contributes to ocular anterior segment dysgenesis in Col4a1 mutant mice.Matrix biology : journal of the International Society for Matrix Biology · 2022
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Regulation of TGF-β Family Signaling by Inhibitory Smads.Cold Spring Harbor perspectives in biology · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Development of astrocytes in the vertebrate eye.Developmental dynamics : an official publication of the American Association of Anatomists · 2014
    Article
  16. Article
  17. Article
  18. The role of heredity in pterygium development.International journal of ophthalmology · 2014
    Review
  19. 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

6 authors at 1 institution in 1 country.

Rui ZhangKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China.
Heng Huang
Peijuan Cao
Zhenzhen Wang
Yan Chen
Yi Pan
Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smad7 is an intracellular inhibitory protein that antagonizes the signaling of TGF-β family members. Deletion of Smad7 in the mouse leads to an abnormality in heart development. However, whether Smad7 has a functional role in the development of other organs has been elusive. Here we present evidence that Smad7 imparts a role to eye development in the mouse. Smad7 is expressed in both the lens and retina in the developing embryonic eye. Depletion of Smad7 caused various degrees of coloboma and microphthalmia with alterations in cell apoptosis and proliferation in eyes. Smad7 was implicated in lens differentiation but was not required for the induction of the lens placode. The development of the periocular mesenchyme was retarded with the down-regulation of Bmp7 and Pitx2 in mutant mice. Retinal spatial patterning was affected by Smad7 deletion and was accompanied by altered bone morphogenetic protein (BMP) signaling. At late gestation stages, TGF-β signaling was up-regulated in the differentiating retina. Smad7 mutant mice displayed an expanded optic disc with increasing of sonic hedgehog (SHH) signaling. Furthermore, loss of Smad7 led to a temporal change in retinal neurogenesis. In conclusion, our study suggests that Smad7 is essential for eye development. In addition, our data indicate that alterations in the signaling of BMP, TGF-β, and SHH likely underlie the defects in eye development caused by Smad7 deletion.

Indexed as

AnimalsBone Morphogenetic Protein 7Cell DifferentiationColobomaDown-RegulationGene DeletionHedgehog ProteinsHomeobox Protein PITX2Homeodomain ProteinsLens, CrystallineMiceMice, Mutant StrainsMicrophthalmosNeurogenesisRetinaSignal Transductionbmp7 protein, mouseBone Morphogenetic Protein 7Hedgehog ProteinsHomeobox Protein PITX2Homeodomain ProteinsShh protein, mouseSmad7 ProteinSmad7 protein, mouseTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID23426374
PMCPMC3624411
OpenAlexW2118453327

What OpenQuestion holds

Textmetadata
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.