Evidence map›Paper›PMID 35012849›Full record

ReviewTrends in cell biology2022

Chromatin basis of the senescence-associated secretory phenotype.

Xue Hao, Chen Wang, Rugang Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
7.6field-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

53 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Anti-aging effects of glycyrrhizin via maintaining Klotho levels.Journal of clinical biochemistry and nutrition · 2026
    Article
  3. Review
  4. Article
  5. Extracellular cGAMP in health and disease.Molecular biomedicine · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Xue HaoImmunology, Microenvironment & Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Chen WangImmunology, Microenvironment & Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Rugang ZhangImmunology, Microenvironment & Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USA. Electronic address: rzhang@wistar.org.
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
STRUCTURAL BASIS FOR EPIGENETICS IN AGING AND LONGEVITYP01AG031862 · NIA · WISTAR INSTITUTE · PI ADAMS, PETER D. · 2008 to 2022
$28.3M
SPORE in Ovarian CancerP50CA228991 · NCI · JOHNS HOPKINS UNIVERSITY · PI Ronny I DRAPKIN, IE-MING SHIH · 2018 to 2026
$20.5M
Mechanistic basis and therapeutic strategies for ARID1A mutation in ovarian cancerR01CA202919 · NCI · WISTAR INSTITUTE · PI Xi Chen, Rugang Zhang · 2016 to 2026
$4.1M
Role of BRCA1 Pathway in Regulating Oncogene-Induced SenescenceR01CA160331 · NCI · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2012 to 2021
$4.0M
Targeting EZH2 in CARM1-expressing epithelial ovarian cancerR01CA163377 · NCI · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2012 to 2021
$3.7M
Regulation of tumor recurrence by stress activated neutrophilsR01CA243142 · NCI · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2020 to 2025
$2.8M
Synthetic lethality based combination approaches to ARID1A mutation in ovarian cancerR01CA239128 · NCI · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2019 to 2024
$2.5M
NCI NIH HHS P30 CA010815NCI NIH HHS P50 CA228991NCI NIH HHS R01 CA160331NCI NIH HHS R01 CA163377NCI NIH HHS R01 CA202919NCI NIH HHS R01 CA239128NCI NIH HHS R01 CA243142NIA NIH HHS P01 AG031862
6 · The paper itself

Abstract

Cellular senescence is a stable cell growth arrest. Senescent cells are metabolically active, as exemplified by the secretion of inflammatory cytokines, chemokines, and growth factors, which is termed senescence-associated secretory phenotype (SASP). The SASP exerts a range of functions in both normal health and pathology, which is possibly best characterized in cancers and physical aging. Recent studies demonstrated that chromatin is instrumental in regulating the SASP both through nuclear transcription and via the innate immune cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway in the cytoplasm. Here, we will review these regulatory mechanisms, with an emphasis on most recent developments in the field. We will highlight the challenges and opportunities in developing intervention approaches, such as targeting chromatin regulatory mechanisms, to alter the SASP as an emerging approach to combat cancers and achieve healthy aging.

Indexed as

ChromatinNeoplasmsCellular SenescenceCytoplasmHumansPhenotypeSenescence-Associated Secretory PhenotypeChromatinchromatin structurecytoplasmic chromatinenhancer–promoter interactionsenescence-associated secretory phenotypesenomorphics

Identifiers

PMID35012849
PMCPMC9106822
OpenAlexW4206396864

What OpenQuestion holds

Textmetadata
LicenceTDM
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.