Evidence map›Paper›PMID 19036896›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2009

Vascular endothelial senescence: from mechanisms to pathophysiology.

Jorge D Erusalimsky

Abstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

201 citing papers in PubMed, 1 synthesis or guideline pooled it.

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141 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

1 author.

Jorge D ErusalimskyCardiff School of Health Sciences, University of Wales Institute, Cardiff CF5 2YB, UK. jderusalimsky@uwic.ac.uk

Funding

British Heart Foundation
6 · The paper itself

Abstract

Most mitotically competent mammalian cell types can react to stress by undergoing a phenotypically distinctive and permanent form of growth arrest called "cellular senescence." This response has been extensively characterized in cell culture and more recently it has been found to occur also in vivo in a number of tissues. In this review I will present the case for the occurrence of senescence in the vascular endothelium. I will also discuss the mechanisms and factors that modulate endothelial cell replicative capacity and the onset of senescence. Finally, I will examine the senescent phenotype and its possible consequences for the development and progression of vascular diseases.

Indexed as

Cell ProliferationCellular SenescenceAnimalsApoptosisAtherosclerosisDNA DamageEndothelium, VascularHumansMitochondriaNeovascularization, PhysiologicOxidative StressReactive Oxygen SpeciesTelomeraseTelomereThrombosisVasodilationReactive Oxygen SpeciesTelomerase

Identifiers

PMID19036896
PMCPMC2636933

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.