Evidence map›Paper›PMID 25330150›Full record

ArticlePloS one2014

Apaf-1 inhibitors protect from unwanted cell death in in vivo models of kidney ischemia and chemotherapy induced ototoxicity.

Mar Orzáez, Mónica Sancho, Sandra Marchán, Laura Mondragón, Rebeca Montava, Juan García Valero, Olatz Landeta, Gorka Basañez, Rodrigo J Carbajo, Antonio Pineda-Lucena and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 30 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

16 authors at 3 institutions in 1 country.

Mar OrzáezLaboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Mónica SanchoLaboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Sandra MarchánLaboratorios SALVAT S.A., Esplugues de Llobregat, Barcelona, Spain.
Laura MondragónLaboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Rebeca MontavaLaboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Juan García ValeroUnidad de Biofísica, CSIC, UPV/EHU, Leioa, Spain.
Olatz LandetaUnidad de Biofísica, CSIC, UPV/EHU, Leioa, Spain.
Gorka BasañezUnidad de Biofísica, CSIC, UPV/EHU, Leioa, Spain.
Rodrigo J CarbajoLaboratory of Structural Biochemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Antonio Pineda-LucenaLaboratory of Structural Biochemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Jordi BujonsDepartment of Chemical and Biomolecular Nanotechnology and Department of Biological Chemistry and Molecular Modeling, Instituto de Química Avanzada de Cataluña (CSIC), Barcelona, Spain.
Alejandra MoureDepartment of Chemical and Biomolecular Nanotechnology and Department of Biological Chemistry and Molecular Modeling, Instituto de Química Avanzada de Cataluña (CSIC), Barcelona, Spain.
Angel MesseguerDepartment of Chemical and Biomolecular Nanotechnology and Department of Biological Chemistry and Molecular Modeling, Instituto de Química Avanzada de Cataluña (CSIC), Barcelona, Spain.
Carmen LagunasLaboratorios SALVAT S.A., Esplugues de Llobregat, Barcelona, Spain.
Carmen HerreroLaboratorios SALVAT S.A., Esplugues de Llobregat, Barcelona, Spain.
Enrique Pérez-PayáLaboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, Valencia, Spain; Instituto de Biomedicina de Valencia (CSIC), Valencia, Spain.
Centro de Investigacion Principe Felipe · ESFundación Biofísica Bizkaia · ESSalvat (Spain) · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExcessive apoptosis induces unwanted cell death and promotes pathological conditions. Drug discovery efforts aimed at decreasing apoptotic damage initially targeted the inhibition of effector caspases. Although such inhibitors were effective, safety problems led to slow pharmacological development. Therefore, apoptosis inhibition is still considered an unmet medical need. METHODOLOGY AND PRINCIPAL

findingsThe interaction between Apaf-1 and the inhibitors was confirmed by NMR. Target specificity was evaluated in cellular models by siRNa based approaches. Cell recovery was confirmed by MTT, clonogenicity and flow cytometry assays. The efficiency of the compounds as antiapoptotic agents was tested in cellular and in vivo models of protection upon cisplatin induced ototoxicity in a zebrafish model and from hypoxia and reperfusion kidney damage in a rat model of hot ischemia.

conclusionsApaf-1 inhibitors decreased Cytc release and apoptosome-mediated activation of procaspase-9 preventing cell and tissue damage in ex vivo experiments and in vivo animal models of apoptotic damage. Our results provide evidence that Apaf-1 pharmacological inhibition has therapeutic potential for the treatment of apoptosis-related diseases.

Indexed as

Hearing LossAnimalsAntineoplastic AgentsApoptosisApoptotic Protease-Activating Factor 1Cell DeathCisplatinDisease Models, AnimalHeLa CellsHeterocyclic Compounds, 4 or More RingsHumansKidneyKidney DiseasesMaleMiceRatsAntineoplastic AgentsAPAF1 protein, humanApaf1 protein, mouseApaf1 protein, ratApoptotic Protease-Activating Factor 1CisplatinHeterocyclic Compounds, 4 or More RingsZebrafish Proteins

Identifiers

PMID25330150
PMCPMC4203855
OpenAlexW2021908472

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.