Evidence map›Paper›PMID 31113906›Full record

ArticleAging2019

Epigenetic clock analysis of human fibroblasts

Mieko Matsuyama, David J WuWong, Steve Horvath, Shigemi Matsuyama

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

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Exposomes to Exosomes: Exosomes as Tools to Study Epigenetic Adaptive Mechanisms in High-Altitude Humans.International journal of environmental research and public health · 2021
    Review
  10. Article
  11. Review
  12. The use of DNA methylation clock in aging research.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  13. Mechanisms of aging, age-associated diseases, and lifespan determination.Experimental biology and medicine (Maywood, N.J.) · 2020
    Article
  14. Current perspectives on the cellular and molecular features of epigenetic ageing.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  15. Analysis of epigenetic agingExperimental biology and medicine (Maywood, N.J.) · 2020
    Review
  16. Article
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 3 institutions in 1 country.

Mieko MatsuyamaDivision of Hematology and Oncology, Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland OH 44106, USA.
David J WuWongDivision of Hematology and Oncology, Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland OH 44106, USA.
Steve HorvathDepartment of Human Genetics and Biostatistics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
Shigemi MatsuyamaDivision of Hematology and Oncology, Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland OH 44106, USA.
Case Western Reserve University · USCase Comprehensive Cancer CenterUniversity of California, Los Angeles · US

Funding

Validation and optimization of epigenetic clocksU01AG060908 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RITZ, BEATE R. · 2018 to 2022
$3.4M
The epiGenetIcs Leads to aGe-relAted diseases (GILGA-mesh) NetworkU34AG051425 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HORVATH, STEVE · 2015 to 2017
$954k
NIA NIH HHS U01 AG060908NIA NIH HHS U34 AG051425
6 · The paper itself

Abstract

Aging is associated with a genome-wide change of DNA methylation (DNAm). "DNAm age" is defined as the predicted chronological age by the age estimator based on DNAm. The estimator is called the epigenetic clock. The molecular mechanism underlining the epigenetic clock is still unknown. Here, we evaluated the effects of hypoxia and two immortalization factors, hTERT and SV40-LargeT (LT), on the DNAm age of human fibroblasts in vitro. We detected the cell division-associated progression of DNAm age after >10 population doublings. Moreover, the progression of DNAm age was slower under hypoxia (1% oxygen) compared to normoxia (21% oxygen), suggesting that oxygen levels determine the speed of the epigenetic aging. We show that the speed of cell division-associated DNAm age progression depends on the chronological age of the cell donor. hTERT expression did not arrest cell division-associated progression of DNAm age in most cells. SV40LT expression produced inconsistent effects, including rejuvenation of DNAm age. Our results show that a) oxygen and the targets of SV40LT (e.g. p53) modulate epigenetic aging rates and b) the chronological age of donor cells determines the speed of mitosis-associated DNAm age progression in daughter cells.

Indexed as

Biological ClocksDNA MethylationAdultAgingAntigens, Polyomavirus TransformingEpigenesis, GeneticFibroblastsHumansHypoxiaInfant, NewbornPrimary Cell CultureTelomeraseAntigens, Polyomavirus TransformingTelomeraseTERT protein, humanDNA methylationepigenetic ageepigenetic clockhypoxiaimmortalization

Identifiers

PMID31113906
PMCPMC6555444
OpenAlexW2945223047

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.