Evidence map›Paper›PMID 30844644›Full record

ArticleRedox biology2019

TRIM69 inhibits cataractogenesis by negatively regulating p53.

Xianfang Rong, Jun Rao, Dan Li, Qinghe Jing, Yi Lu, Yinghong Ji

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  3. TRIM69 alleviates ultraviolet B irradiation-induced ferroptosis by regulating p53 in human lens epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
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  14. Trim69 is a microtubule regulator that acts as a pantropic viral inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

6 authors at 4 institutions in 1 country.

Xianfang RongDepartment of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; Eye Institute, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; National Health Commission (NHC) Key Laboratory of Myopia (Fudan University), No. 83 Fenyang Road, Shanghai, 200031, China; Laboratory of Myopia, Chinese Academy of Medical Sciences, No. 83 Fenyang Road, Shanghai, 200031, China; Key Laboratory of Visual Impairment and Restoration of Shanghai, No. 83 Fenyang Road, Shanghai, 200031, China.
Jun RaoJiangxi Provincial Key Laboratory of Translational Medicine and Oncology, Jiangxi Cancer Hospital, Jiangxi Cancer Center, Nanchang, 330029, China.
Dan LiDepartment of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; Eye Institute, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; National Health Commission (NHC) Key Laboratory of Myopia (Fudan University), No. 83 Fenyang Road, Shanghai, 200031, China; Laboratory of Myopia, Chinese Academy of Medical Sciences, No. 83 Fenyang Road, Shanghai, 200031, China; Key Laboratory of Visual Impairment and Restoration of Shanghai, No. 83 Fenyang Road, Shanghai, 200031, China.
Qinghe JingDepartment of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; Eye Institute, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; National Health Commission (NHC) Key Laboratory of Myopia (Fudan University), No. 83 Fenyang Road, Shanghai, 200031, China; Laboratory of Myopia, Chinese Academy of Medical Sciences, No. 83 Fenyang Road, Shanghai, 200031, China; Key Laboratory of Visual Impairment and Restoration of Shanghai, No. 83 Fenyang Road, Shanghai, 200031, China.
Yi LuDepartment of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; Eye Institute, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; National Health Commission (NHC) Key Laboratory of Myopia (Fudan University), No. 83 Fenyang Road, Shanghai, 200031, China; Laboratory of Myopia, Chinese Academy of Medical Sciences, No. 83 Fenyang Road, Shanghai, 200031, China; Key Laboratory of Visual Impairment and Restoration of Shanghai, No. 83 Fenyang Road, Shanghai, 200031, China.
Yinghong JiDepartment of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; Eye Institute, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China; National Health Commission (NHC) Key Laboratory of Myopia (Fudan University), No. 83 Fenyang Road, Shanghai, 200031, China; Laboratory of Myopia, Chinese Academy of Medical Sciences, No. 83 Fenyang Road, Shanghai, 200031, China; Key Laboratory of Visual Impairment and Restoration of Shanghai, No. 83 Fenyang Road, Shanghai, 200031, China. Electronic address: yinghong_ji@163.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNEye & ENT Hospital of Fudan University · CNJiangxi Provincial Cancer Hospital · CNNational Health and Family Planning Commission · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ultraviolet B (UVB) irradiation can induce reactive oxygen species (ROS) production and apoptosis in human lens epithelial cells (HLECs), thus leading to the formation of cataracts. We studied the role of tripartite motif 69 (TRIM69) in cataract formation. The expression of TRIM69 protein was down-regulated in both human cataract capsule tissues and HLECs treated with UVB, whereas the expression of p53 protein exhibited an opposite trend. Ectopic expression of TRIM69 in HLECs significantly suppressed UVB-induced apoptosis and ROS production, whereas knockdown of TRIM69 promoted apoptosis and ROS production. TRIM69 can interact with p53 and induce its ubiquitination. The effects of TRIM69 overexpression in UVB-induced cell apoptosis and ROS production was clearly weakened by p53 overexpression, thus suggesting a role for p53 in TRIM69 functions. Furthermore, inhibition of ROS mitigated the effects of UVB irradiation on ROS production, cell apoptosis, forkhead box protein 3a (Foxo3a) phosphorylation, and TRIM69 expression. Additionally, Foxo3a overexpression significantly enhanced TRIM69 promoter activity, whereas Foxo3a knockdown had the opposite effect. In conclusion, we provide the first demonstration that Foxo3a is a potential transcription factor for TRIM69, and TRIM69 induces p53 ubiquitination. These results suggest that the Foxo3a/TRIM69/p53 regulatory network may be involved in cataract formation.

Indexed as

Gene Expression RegulationApoptosisCataractEpithelial CellsHumansProtein BindingReactive Oxygen SpeciesTripartite Motif ProteinsTumor Suppressor Protein p53UbiquitinationUbiquitin-Protein LigasesUltraviolet RaysReactive Oxygen SpeciesTP53 protein, humanTRIM69 protein, humanTripartite Motif ProteinsTumor Suppressor Protein p53Ubiquitin-Protein LigasesCataractFoxo3ap53TRIM69UVB

Identifiers

PMID30844644
PMCPMC6402377
OpenAlexW2920758895

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.