Evidence map›Paper›PMID 7479963›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Telomere length and replicative aging in human vascular tissues.

E Chang, C B Harley

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 2 pooled it
8.3field-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

161 citing papers in PubMed, 2 syntheses or guidelines pooled it, 630 citations in OpenAlex.

  1. Telomere Biology and Thoracic Aortic Aneurysm.International journal of molecular sciences · 2017
    Pooled it
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  12. Therapeutic targeting of telomerase ameliorates experimental choroidal neovascularization.Biochimica et biophysica acta. Molecular basis of disease · 2024
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101 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

E ChangGeron Corp., Menlo Park, CA 94025, USA.
C B Harley
Geron (United States) · US

Funding

STRUCTURE/FUNCTION OF TELOMERES IN MAMMALIAN AGINGR37AG009383 · NIA · JOHNS HOPKINS UNIVERSITY · PI GREIDER, CAROL W · 1997 to 2016
$6.1M
STRUCTURE AND FUNCTION OF TELOMERES IN MAMMALIAN AGINGR01AG009383 · NIA · COLD SPRING HARBOR LABORATORY · PI GREIDER, CAROL W · 1991 to 1996
–
NIA NIH HHS AG-09383
6 · The paper itself

Abstract

Because repeated injury of the endothelium and subsequent turnover of intimal and medial cells have been implicated in atherosclerosis, we examined telomere length, a marker of somatic cell turnover, in cells from these tissues. Telomere lengths were assessed by Southern analysis of terminal restriction fragments (TRFs) generated by HinfI/Rsa I digestion of human genomic DNA. Mean TRF length decreased as a function of population doublings in human endothelial cell cultures from umbilical veins, iliac arteries, and iliac veins. When endothelial cells were examined for mean TRF length as a function of donor age, there was a significantly greater rate of decrease for cells from iliac arteries than from iliac veins (102 bp/yr vs. 47 bp/yr, respectively, P < 0.05), consistent with higher hemodynamic stress and increased cell turnover in arteries. Moreover, the rate of telomere loss as a function of donor age was greater in the intimal DNA of iliac arteries compared to that of the internal thoracic arteries (147 bp/yr vs. 87 bp/yr, respectively, P < 0.05), a region of the arterial tree subject to less hemodynamic stress. This indicates that the effect is not tissue specific. DNA from the medial tissue of the iliac and internal thoracic arteries showed no significant difference in the rates of decrease, suggesting that chronic stress leading to cellular senescence is more pronounced in the intima than in the media. These observations extend the use of telomere size as a marker for the replicative history of cells and are consistent with a role for focal replicative senescence in cardiovascular diseases.

Indexed as

Cellular SenescenceAdolescentAdultAgedCell DivisionChild, PreschoolEndothelium, VascularFemaleHemodynamicsHumansIliac ArteryMaleMiddle AgedStress, MechanicalTelomereThoracic Arteries

Identifiers

PMID7479963
PMCPMC40597
OpenAlexW2035963497

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.