Evidence map›Paper›PMID 39518943›Full record

ArticleInternational journal of molecular sciences2024

Pharmacological Preconditioning with Fenofibrate in Cardiomyocyte Cultures of Neonatal Rats Subjected to Hypoxia/Reoxygenation, High Glucose, and Their Combination.

Víctor Hugo Oidor-Chan, Araceli Sánchez-López, Agustina Cano-Martinez, Willy Ramses García-Niño, Elizabeth Soria-Castro, Leonardo Del Valle-Mondragón, Gabriela Zarco-Olvera, Mariana Patlán, Veronica Guarner-Lans, Emma Rodríguez-Maldonado and 3 more

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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Víctor Hugo Oidor-ChanDepartment of Biotechnology, Autonomous Metropolitan University, Iztapalapa Campus, Av. Ferrocarril de San Rafael Atlixco 186, Col. Leyes de Reforma 1ª. Sección, Alcaldía Iztapalapa, Mexico City 09310, Mexico.ORCID 0000-0002-8910-5671
Araceli Sánchez-LópezDepartment of Pharmacobiology, Center for Research and Advanced Studies of the National Polytechnic Institute, Calz. de los Tenorios 235, Col Granjas Coapa, Tlalpan, Mexico City 14330, Mexico.
Agustina Cano-MartinezDepartment of Physiology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.ORCID 0000-0002-6703-2176
Willy Ramses García-NiñoDepartment of Cardiovascular Biomedicine, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.ORCID 0000-0003-4865-6933
Elizabeth Soria-CastroDepartment of Cardiovascular Biomedicine, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.ORCID 0000-0001-8050-1961
Leonardo Del Valle-MondragónDepartment of Pharmacology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.ORCID 0000-0002-2999-1050
Gabriela Zarco-OlveraDepartment of Pharmacology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.
Mariana PatlánSubdirection of Basic and Technological Research, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.ORCID 0000-0002-6660-7388
Veronica Guarner-LansDepartment of Physiology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.
Emma Rodríguez-MaldonadoLaboratory of Cell Biology, Department of Physiology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.
Javier Flores-EstradaDivision of Investigation, Juarez Hospital of Mexico, Av. Instituto Politecnico Nacional No. 5160, Magdalena de las Salinas, Gustavo A. Madero, Mexico City 07760, Mexico.ORCID 0000-0002-7029-7036
Vicente Castrejón-TéllezDepartment of Physiology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.
Luz Ibarra-LaraDepartment of Pharmacology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological preconditioning is an alternative to protect the heart against the consequences of damage from ischemia/reperfusion (I/R). It is based on the administration of specific drugs that imitate the effect of ischemic preconditioning (IPC). Peroxisomal proliferator-activated receptors (PPARs) can prevent apoptosis in pathologies such as I/R and heart failure. Therefore, our objective was to determine if the stimulation of PPARα with fenofibrate (feno) decreases the apoptotic process induced by hypoxia/reoxygenation (HR), high glucose (HG), and HR/HG. For that purpose, cardiomyocyte cultures were divided into the following groups: Group 1-control (Ctrl); Group 2-HR; Group 3-HR + 10 μM feno; Group 4-HG, (25 mM glucose); Group 5-HG + feno; Group 6-HR/HG, and Group 7-HR/HG + feno. Our results indicate that cell viability decreases in neonatal cardiomyocytes undergoing HR, HG, and their combination, while feno improved cell viability. Feno treatment decreased apoptosis compared with HG-, HR-, or HG/HR-vehicle-treated. Nuclear- and mitochondrial-apoptosis markers increased in neonatal cardiomyocytes from HR, HG, and HR/HG; while the cytotoxicity decreased in cells treated with feno. In addition, the expression of Bax, Bad, and caspase 9 decreased due to feno, while 14-3-3ɛ and Bcl2 were increased. Inner mitochondrial cytochrome C increased with feno in every condition, as well as mitochondrial activity. Feno treatment prevented injury in the ultrastructure and in the mitochondrial membranes. Thus, our results suggest that feno decreases apoptosis in neonatal cardiomyocytes, improving the ultrastructure of mitochondria in the pathological conditions studied.

Indexed as

Animals, NewbornApoptosisCell SurvivalFenofibrateGlucoseMyocytes, CardiacAnimalsCell HypoxiaCells, CulturedMyocardial Reperfusion InjuryPPAR alphaRatsRats, WistarFenofibrateGlucosePPAR alphaapoptosisfenofibratehigh glucosehypoxia-reoxygenationpharmacological preconditioning

Identifiers

PMID39518943
PMCPMC11547148

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.