Evidence map›Paper›PMID 32169084›Full record

ArticleCell communication and signaling : CCS2020

Copper induce zebrafish retinal developmental defects via triggering stresses and apoptosis.

Guang Zhao, HaoJie Sun, Ting Zhang, Jing-Xia Liu

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Review
  3. Disrupted Copper Homeostasis and Impaired Retinal Development Caused byAnimals : an open access journal from MDPI · 2026
    Article
  4. Article
  5. Review
  6. Identification and Validation of DLD as a Cuproptosis-Associated Biomarker in Preeclampsia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Role of cuproptosis in digestive system tumors (Review).International journal of molecular medicine · 2026
    Review
  9. Article
  10. Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Article
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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

4 authors at 1 institution in 1 country.

Guang ZhaoCollege of Fisheries, Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, 430070, China.
HaoJie SunCollege of Fisheries, Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, 430070, China.
Ting ZhangCollege of Fisheries, Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, 430070, China.
Jing-Xia LiuCollege of Fisheries, Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, 430070, China. ichliu@mail.hzau.edu.cn.
Huazhong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe disorder of copper homeostasis is linked with disease and developmental defects, and excess copper_nanoparticles (CuNPs) and ion (Cu

methodsEmbryos were stressed with copper (CuNPs and Cu

resultsCopper reduced retinal cells and down-regulated expression of retinal genes, damaged the structures of ER and mitochondria in retinal cells, up-regulated unfold protein responses (UPR) and ROS, and increased apoptosis in copper-stressed retinal cells. The copper induced retinal defects could be significantly neutralized by ROS scavengers reduced Glutathione (GSH) & N-acetylcysteine (NAC) and ER stress inhibitor 4- phenylbutyric acid (PBA). Blocking the transportation of copper to mitochondria, or to trans-Golgi network and to be exported into plasma, by deleting gene cox17 or atp7a, could alleviate retinal developmental defects in embryos under copper stresses.

conclusionsThis is probably the first report to reveal that copper nanoparticles and ions induce retinal developmental defects via upregulating UPR and ROS, leading to apoptosis in zebrafish embryonic retinal cells. Integrated function of copper transporter (Cox17 and Atp7a) is necessary for copper induced retinal defects.

Indexed as

RetinaZebrafishAnimalsApoptosisCell ProliferationCopperEndoplasmic ReticulumMitochondriaReactive Oxygen SpeciesUnfolded Protein ResponseCopperReactive Oxygen SpeciesApoptosisatp7acox17ERRetinaROS

Identifiers

PMID32169084
PMCPMC7071659
OpenAlexW3012085768

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.