Evidence map›Paper›PMID 34482802›Full record

ArticleBioengineered2021

Coordination of PRKCA/PRKCA-AS1 interplay facilitates DNA methyltransferase 1 recruitment on DNA methylation to affect protein kinase C alpha transcription in mitral valve of rheumatic heart disease.

Zan Xie, Qianli Wang, Shaojuan Hu

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026
    Review
  2. Study on the expression of lncRNATranslational cancer research · 2024
    Article
  3. Review
  4. Article
  5. LncRNA-mediated DNA methylation: an emerging mechanism in cancer and beyond.Journal of experimental & clinical cancer research : CR · 2022
    Review
  6. Article
  7. Review
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

3 authors at 2 institutions in 1 country.

Zan XieDepartment of Cardiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai City, China.
Qianli WangCardiovascular Surgery Intensive Care Unit, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai City, China.
Shaojuan HuCardiovascular Surgery Intensive Care Unit, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai City, China.
Yuhuangding Hospital · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study, mitral valve tissues from three mitral stenosis patients with RHD by valve replacement and two healthy donors were harvested and conducted DNA methylation signature on PRKCA by MeDIP-qPCR. The presence of hypomethylated CpG islands at promoter and 5' terminal of PRKCA was observed in RHD accompanied with highly expressed PRKCA and down-regulated antisense long non-coding RNA (lncRNA) PRKCA-AS1 compared to health control. Furthermore, the enrichments of DNMT1/3A/3B on PRKCA were detected by ChIP-qPCR assay

Indexed as

Rheumatic Heart DiseaseAgedDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationFemaleHumansMaleMiddle AgedMitral ValvePromoter Regions, GeneticProtein Kinase C-alphaRNA, Long NoncodingDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanPRKCA protein, humanProtein Kinase C-alphaRNA, Long Noncodingdna methylationdnmt1prkca-as1protein kinase c alphaRheumatic heart disease

Identifiers

PMID34482802
PMCPMC8806685
OpenAlexW3196766252

What OpenQuestion 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 OpenQuestion graph.