Evidence map›Paper›PMID 34362460›Full record

ArticleBiological research2021

DNMT1-mediated PPARα methylation aggravates damage of retinal tissues in diabetic retinopathy mice.

Ying Zhu, Xinru Wang, Xiaoyun Zhou, Lexi Ding, Dan Liu, Huizhuo Xu

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. New perspectives on DNA methylation modifications in ocular diseases.International journal of ophthalmology · 2025
    Review
  7. Article
  8. Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024
    Review
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  10. Article
  11. Review
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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 3 institutions in 1 country.

Ying ZhuEye Center of Xiangya Hospital, Central South University, No. 87 Xiangya Road, Hunan, 410008, Changsha, China.
Xinru WangEye Center of Xiangya Hospital, Central South University, No. 87 Xiangya Road, Hunan, 410008, Changsha, China.
Xiaoyun ZhouDepartment of Ophthalmology, The First Hospital of Changsha, 311 Yingpan Road, Hunan, Changsha, China.
Lexi DingEye Center of Xiangya Hospital, Central South University, No. 87 Xiangya Road, Hunan, 410008, Changsha, China.
Dan LiuEye Center of Xiangya Hospital, Central South University, No. 87 Xiangya Road, Hunan, 410008, Changsha, China.
Huizhuo XuEye Center of Xiangya Hospital, Central South University, No. 87 Xiangya Road, Hunan, 410008, Changsha, China. xuhzhuo@163.com.
Xiangya Hospital Central South University · CNCentral South University · CNThe First Hospital of Changsha · CN

Funding

National Natural Science Foundation of China 81600756
6 · The paper itself

Abstract

backgroundPeroxisome proliferator-activated receptor alpha (PPARα) is associated with diabetic retinopathy (DR), and the underlying mechanism is still unclear. Aim of this work was to investigate the mechanism of PPARα in DR.

methodsHuman retinal capillary pericytes (HRCPs) were treated with high glucose (HG) to induce DR cell model. DR mouse model was established by streptozotocin injection, and then received 5-Aza-2-deoxycytidine (DAC; DNA methyltransferase inhibitor) treatment. Hematoxylin-eosin staining was performed to assess retinal tissue damage. PPARα methylation was examined by Methylation-Specific PCR. Flow cytometry and DCFH-DA fluorescent probe was used to estimate apoptosis and reactive oxygen species (ROS). The interaction between DNA methyltransferase-1 (DNMT1) and PPARα promoter was examined by Chromatin Immunoprecipitation. Quantitative real-time PCR and western blot were performed to assess gene and protein expression.

resultsHG treatment enhanced the methylation levels of PPARα, and repressed PPARα expression in HRCPs. The levels of apoptotic cells and ROS were significantly increased in HRCPs in the presence of HG. Moreover, DNMT1 was highly expressed in HG-treated HRCPs, and DNMT1 interacted with PPARα promoter. PPARα overexpression suppressed apoptosis and ROS levels of HRCPs, which was rescued by DNMT1 up-regulation. In DR mice, DAC treatment inhibited PPARα methylation and reduced damage of retinal tissues.

conclusionDNMT1-mediated PPARα methylation promotes apoptosis and ROS levels of HRCPs and aggravates damage of retinal tissues in DR mice. Thus, this study may highlight novel insights into DR pathogenesis.

Indexed as

Diabetic RetinopathyAnimalsApoptosisCells, CulturedDiabetes MellitusDisease Models, AnimalDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationHumansMethylationMicePPAR alphaPromoter Regions, GeneticRetinaDNA (Cytosine-5-)-Methyltransferase 1Dnmt1 protein, mousePPAR alphaApoptosisDiabetic retinopathyDNA methylationDNMT1PPARα

Identifiers

PMID34362460
PMCPMC8348846
OpenAlexW3188396347

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.