Evidence map›Paper›PMID 33539668›Full record

ArticleAging cell2021

ATF3 drives senescence by reconstructing accessible chromatin profiles.

Chao Zhang, Xuebin Zhang, Li Huang, Yiting Guan, Xiaoke Huang, Xiao-Li Tian, Lijun Zhang, Wei Tao

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Chromatin accessibility regulates age-dependent nuclear mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026
    Review
  10. Review
  11. Review
  12. ATF3 Deficiency Exacerbates Ageing-Induced Atherosclerosis and Clinical Intervention Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
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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

8 authors at 2 institutions in 1 country.

Chao ZhangThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.ORCID 0000-0003-4167-4872
Xuebin ZhangThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.ORCID 0000-0002-0563-6994
Li HuangThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.
Yiting GuanThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.
Xiaoke HuangThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.
Xiao-Li TianDepartment of Human Population Genetics, Human Aging Research Institute (HARI) and School of Life Sciences, Nanchang University, Nanchang, China.ORCID 0000-0002-0868-7025
Lijun ZhangThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.
Wei TaoThe MOE Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing, China.
Peking University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromatin organization and transcriptional profiles undergo tremendous reordering during senescence. However, uncovering the regulatory mechanisms between chromatin reconstruction and gene expression in senescence has been elusive. Here, we depicted the landscapes of both chromatin accessibility and gene expression to reveal gene regulatory networks in human umbilical vein endothelial cell (HUVEC) senescence and found that chromatin accessibilities are redistributed during senescence. Particularly, the intergenic chromatin was massively shifted with the increased accessibility regions (IARs) or decreased accessibility regions (DARs), which were mainly enhancer elements. We defined AP-1 transcription factor family as being responsible for driving chromatin accessibility reconstruction in IARs, where low DNA methylation improved binding affinity of AP-1 and further increased the chromatin accessibility. Among AP-1 transcription factors, we confirmed ATF3 was critical to reconstruct chromatin accessibility to promote cellular senescence. Our results described a dynamic landscape of chromatin accessibility whose remodeling contributes to the senescence program, we identified that AP-1 was capable of reorganizing the chromatin accessibility profile to regulate senescence.

Indexed as

Cellular SenescenceActivating Transcription Factor 3ChromatinDNA MethylationGene Expression RegulationGene Regulatory NetworksGenome, HumanHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsTranscription Factor AP-1Transcription, GeneticActivating Transcription Factor 3ChromatinTranscription Factor AP-1AP-1ATF3chromatin accessibilityDARsDNA methylationheterochromatinIARssenescence

Identifiers

PMID33539668
PMCPMC7963335
OpenAlexW3127751237

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.