Evidence map›Paper›PMID 24799429›Full record

ArticleAging2014

Oxidative stress and antioxidant response in fibroblasts from Werner and atypical Werner syndromes.

Marta Seco-Cervera, Marta Spis, José Luis García-Giménez, José Santiago Ibañez-Cabellos, Ana Velázquez-Ledesma, Isabel Esmorís, Sergio Bañuls, Giselle Pérez-Machado, Federico V Pallardó

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

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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

9 authors at 6 institutions in 2 countries.

Marta Seco-CerveraCIBERER. Centro de Investigación Biomédica en Red de Enfermedades Raras, Valencia, Spain.
Marta Spis
José Luis García-Giménez
José Santiago Ibañez-Cabellos
Ana Velázquez-Ledesma
Isabel Esmorís
Sergio Bañuls
Giselle Pérez-Machado
Federico V PallardóDepartment of Physiology, Medicine School, University of Valencia, Valencia. Spain.
Universitat de València · ESCentre for Biomedical Network Research on Rare Diseases · ESCentro de Investigación Biomédica en Red · ESINCLIVA Health Research Institute · ESSistemas Genómicos · ESUniversidad Central "Marta Abreu" de las Villas (UCLV) · CU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Werner Syndrome (WS, ICD-10 E34.8, ORPHA902) and Atypical Werner Syndrome (AWS, ICD-10 E34.8, ORPHA79474) are very rare inherited syndromes characterized by premature aging. While approximately 90% of WS individuals have any of a range of mutations in theWRN gene, there exists a clinical subgroup in which the mutation occurs in the LMNA/C gene in heterozygosity. Although both syndromes exhibit an age-related pleiotropic phenotype, AWS manifests the onset of the disease during childhood, while major symptoms in WS appear between the ages of 20 and 30. To study the molecular mechanisms of progeroid diseases provides a useful insight into the normal aging process. Main changes found were the decrease in Cu/Zn and Mn SOD activities in the three cell lines. In AWS, both mRNA SOD and protein levels were also decreased. Catalase and glutathione peroxidases decrease, mainly in AWS. Glutaredoxin (Grx) and thioredoxin (Trx) protein expression was lower in the three progeroid cell lines. Grx and Trx were subjected to post-transcriptional regulation, because protein expression was reduced although mRNA levels were not greatly affected in WS. Low antioxidant defense and oxidative stress occur simultaneously in these rare genetic instability disorders at the onset of progeroid disease.

Indexed as

Oxidative StressAdolescentAdultAging, PrematureAntioxidantsCase-Control StudiesCell LineCell ProliferationChildExodeoxyribonucleasesFemaleFibroblastsGlutathioneHumansLamin Type AMaleAntioxidantsExodeoxyribonucleasesGlutathioneLamin Type ALMNA protein, humanRecQ HelicasesRNA, MessengerSOD1 protein, humanSuperoxide DismutaseSuperoxide Dismutase-1Superoxide Dismutase 2Werner Syndrome HelicaseWRN protein, human

Identifiers

PMID24799429
PMCPMC4012939
OpenAlexW2157686116

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.