Evidence map›Paper›PMID 32283543›Full record

ArticleAging2020

DNA N

Ye Guo, Yuqing Pei, Kexin Li, Wei Cui, Donghong Zhang

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Serum Folate and Vitamin BDiabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  8. Article
  9. Article
  10. Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome.International journal of molecular sciences · 2023
    Review
  11. Article
  12. DNA NTrends in genetics : TIG · 2022
    Review
  13. Novel methylation mark and essential hypertension.Journal, genetic engineering & biotechnology · 2022
    Review
  14. Review
  15. Article
  16. N6-Adenosine Methylation (mJournal of cardiovascular translational research · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Ye GuoDepartment of Laboratory Medicine, Peking Union Medical College Hospital and Peking Union Medical College, Beijing 100021, PR China.
Yuqing PeiState Key Laboratory of Molecular Oncology, Department of Clinical Laboratory, National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, PR China.
Kexin LiState Key Laboratory of Molecular Oncology, Department of Clinical Laboratory, National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, PR China.
Wei CuiState Key Laboratory of Molecular Oncology, Department of Clinical Laboratory, National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, PR China.
Donghong ZhangCenter for Molecular and Translational Medicine, Georgia State University, Research Science Center, Atlanta, GA 30303, USA.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNGeorgia State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation has a role in the pathogenesis of essential hypertension. DNA N6-methyladenine (6mA) modification as a novel adenine methylation exists in human tissues, but whether it plays a role in hypertension development remains unclear. Here, we reported that the global 6mA DNA level in leukocytes was significantly reduced in patients with hypertension and was reversed with successful treatment. Age, systolic blood pressure, and serum total cholesterol and high-density lipoprotein levels were associated with decreased leukocyte 6mA DNA level. Elevated ALKBH1 (AlkB homolog 1), a demethylase of 6mA, level mediated this dynamic change in 6mA level in leukocytes and vascular smooth muscle cells in hypertension mouse and rat models. Knockdown of ALKBH1 suppressed angiotensin II-induced vascular smooth muscle phenotype transformation, proliferation and migration. ALKBH1-6mA directly and negatively regulated hypoxia inducible factor 1 α (HIF1α), which responded to angiotensin II-induced vascular remodeling. Collectively, our results demonstrate a potential epigenetic role for ALKBH1-6mA regulation in hypertension development, diagnosis and treatment.

Indexed as

HypertensionAdenineAlkB Homolog 1, Histone H2a DioxygenaseAngiotensin IIAnimalsDNA MethylationDNA Repair EnzymesEpigenesis, GeneticLeukocytesMiceMuscle, Smooth, VascularRatsVascular Remodeling6-methyladenineAdenineAlkbh1 protein, mouseAlkB Homolog 1, Histone H2a DioxygenaseAngiotensin IIDNA Repair EnzymesALKBH1HIF1αhypertensionN6-methyladeninevascular smooth muscle cells

Identifiers

PMID32283543
PMCPMC7185115
OpenAlexW3016113114

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.