Evidence map›Paper›PMID 39337378›Full record

ArticleInternational journal of molecular sciences2024

Replicative Endothelial Cell Senescence May Lead to Endothelial Dysfunction by Increasing the BH2/BH4 Ratio Induced by Oxidative Stress, Reducing BH4 Availability, and Decreasing the Expression of eNOS.

Ignacio Hernandez-Navarro, Laura Botana, Javier Diez-Mata, Laura Tesoro, Beatriz Jimenez-Guirado, Claudia Gonzalez-Cucharero, Nunzio Alcharani, Jose Luis Zamorano, Marta Saura, Carlos Zaragoza

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

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

  1. Pooled it
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  9. Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026
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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

10 authors.

Ignacio Hernandez-NavarroUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-4331-534X
Laura BotanaUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-2652-9880
Javier Diez-MataUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0001-6520-4416
Laura TesoroUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-1536-4216
Beatriz Jimenez-GuiradoUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.
Claudia Gonzalez-CuchareroUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.
Nunzio AlcharaniUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-9477-7712
Jose Luis ZamoranoCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain.
Marta SauraCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain.ORCID 0000-0002-3977-6581
Carlos ZaragozaUnidad Mixta de Investigación Cardiovascular Universidad Francisco de Vitoria, Hospital Universitario Ramón y Cajal (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-1706-8592

Funding

NIMHD NIH HHS L60 MD007223
6 · The paper itself

Abstract

Vascular aging is associated with the development of cardiovascular complications, in which endothelial cell senescence (ES) may play a critical role. Nitric oxide (NO) prevents human ES through inhibition of oxidative stress, and inflammatory signaling by mechanisms yet to be elucidated. Endothelial cells undergo an irreversible growth arrest and alter their functional state after a finite number of divisions, a phenomenon called replicative senescence. We assessed the contribution of NO during replicative senescence of human aortic (HAEC) and coronary (CAEC) endothelial cells, in which accumulation of the senescence marker SA-β-Gal was quantified by β-galactosidase staining on cultured cells. We found a negative correlation in passaged cell cultures from P0 to P12, between a reduction in NO production with increased ES and the formation of reactive oxygen (ROS) and nitrogen (ONOO

Indexed as

Cellular SenescenceEndothelial CellsNitric OxideNitric Oxide Synthase Type IIIOxidative StressAortaCells, CulturedHumansReactive Oxygen SpeciesNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanReactive Oxygen SpeciesCyclophilin A (CypA)endothelial nitric oxide synthase (eNOS) uncouplingendothelial senescence (ES)extracellular matrix metalloprotease inducer (EMMPRIN)inflammationnitric oxide (NO)oxidative stresstetrahydrobiopterin (BH4)

Identifiers

PMID39337378
PMCPMC11432946

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.