Evidence map›Paper›PMID 33148012›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2021

Prenatal indole-3-carbinol administration activates aryl hydrocarbon receptor-responsive genes and attenuates lung injury in a bronchopulmonary dysplasia model.

Gabriela Guzmán-Navarro, Mario Bermúdez de León, Irene Martín-Estal, Raquel Cuevas-Díaz Durán, Laura Villarreal-Alvarado, Anakaren Vaquera-Vázquez, Tania Cuevas-Cerda, Karina Garza-García, Luis Eduardo Cuervo-Pérez, Álvaro Barbosa-Quintana and 3 more

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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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

13 authors at 2 institutions in 1 country.

Gabriela Guzmán-NavarroTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Mario Bermúdez de LeónDepartamento de Biología Molecular, Centro de Investigación Biomédica del Noreste, Instituto Mexicano del Seguro Social, Monterrey 64720, Mexico.
Irene Martín-EstalTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Raquel Cuevas-Díaz DuránTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Laura Villarreal-AlvaradoTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Anakaren Vaquera-VázquezTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Tania Cuevas-CerdaTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Karina Garza-GarcíaTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Luis Eduardo Cuervo-PérezHospital San José, Sistema de Salud del Tecnológico de Monterrey, Monterrey 64710, Mexico.
Álvaro Barbosa-QuintanaHospital San José, Sistema de Salud del Tecnológico de Monterrey, Monterrey 64710, Mexico.
José Eduardo Pérez-SaucedoTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.
Víctor J Lara-DíazTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.ORCID 0000-0002-1498-8561
Fabiola Castorena-TorresTecnológico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey 64710, Mexico.ORCID 0000-0002-1157-0004
Tecnológico de Monterrey · MXMexican Social Security Institute · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperoxia-hypoxia exposure is a proposed cause of alveolar developmental arrest in bronchopulmonary dysplasia in preterm infants, where mitochondrial reactive oxygen species and oxidative stress vulnerability are increased. The aryl hydrocarbon receptor (AhR) is one of the main activators of the antioxidant enzyme system that protects tissues and systems from damage. The present study aimed to determine if the activation of the AhR signaling pathway by prenatal administration of indole-3-carbinol (I3C) protects rat pups from hyperoxia-hypoxia-induced lung injury. To assess the activation of protein-encoding genes related to the AhR signaling pathway (

Indexed as

AnimalsAnimals, NewbornBronchopulmonary DysplasiaCytokinesDisease Models, AnimalFemaleFibrosisHyperoxiaHypoxiaIndolesInflammation MediatorsLungLung InjuryPregnancyPrenatal Exposure Delayed EffectsRatsCytokinesindole-3-carbinolIndolesInflammation MediatorsReceptors, Aryl HydrocarbonRNA, Messengeraryl hydrocarbon receptorBronchopulmonary dysplasiahyperoxia–hypoxiaindole-3-carbinolmurine modelnewborns

Identifiers

PMID33148012
PMCPMC7988727
OpenAlexW3096064992

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.