Evidence map›Paper›PMID 23478256›Full record

ReviewNature reviews. Cardiology2013

The roles of senescence and telomere shortening in cardiovascular disease.

Frej Fyhrquist, Outi Saijonmaa, Timo Strandberg

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 3 pooled it
23.8field-weighted citation impact, top 1% 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

167 citing papers in PubMed, 3 syntheses or guidelines pooled it, 371 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Observational
  9. Article
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  12. Article
  13. Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Impact of night shift work on telomere length and epigenetic age in older workers.Journal of occupational medicine and toxicology (London, England) · 2025
    Article
  19. Article
  20. Review

107 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Frej FyhrquistMinerva Institute for Medical Research, Biomedicum U2 Helsinki, 00290 Helsinki, Finland. frej.fyhrquist@ helsinki.fi
Outi Saijonmaa
Timo Strandberg
Minerva Foundation · FIHelsinki University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence, defined as arrest during the cell cycle (G₀), is involved in the complex process of the biological ageing of tissues, organs, and organisms. Senescence is driven by many factors including oxidative stress, the DNA damage and repair response, inflammation, mitogenic signals, and telomere shortening. Telomeres are shortened by each cell division until a critical length is reached and dysfunction ensues. DNA-repair pathways are then recruited and cells enter senescence, losing their capacity to proliferate. In addition to cell division, factors causing telomere shortening include DNA damage, inflammation, and oxidative stress. Both cardiovascular risk factors and common cardiovascular diseases, such as atherosclerosis, heart failure, and hypertension, are associated with short leucocyte telomeres, but causality remains undetermined. Telomere length does not satisfy strict criteria for being a biomarker of ageing, but adds predictive power to that of chronological age, and can be considered a marker of cardiovascular ageing. The 'senescence-associated secretory phenotype' of senescent cells exerts a wide range of autocrine and paracrine activities aimed at tissue repair, but which also fuel degenerative and proliferative alterations that contribute to cardiovascular disease. In this Review, the relationship between telomere shortening, senescence, and cardiovascular disease is discussed.

Indexed as

Cellular SenescenceTelomere ShorteningCardiovascular DiseasesGenetic Predisposition to DiseaseHumansMalePhenotypeTelomere

Identifiers

PMID23478256
OpenAlexW2049680139

What OpenQuestion holds

Textmetadata
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.