Evidence map›Paper›PMID 40507872›Full record

ArticleInternational journal of molecular sciences2025

Morphological Alterations of Conal Ridges and Differential Expression of AP2α in the Offspring Hearts of Experimental Diabetic Rats.

Tania Cristina Ramírez-Fuentes, Ricardo Jaime-Cruz, Carlos César Patiño-Morales, Laura Villavicencio-Guzmán, Juan Carlos Corona, María Cristina Revilla-Monsalve, Rosa Adriana Jarillo-Luna, Marcela Salazar-García

Abstract read
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Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Tania Cristina Ramírez-FuentesResearch Laboratory of Developmental Biology and Experimental Teratogenesis, Children's Hospital of México Federico Gomez, Mexico City 06720, Mexico.ORCID 0000-0003-4317-0942
Ricardo Jaime-CruzResearch Laboratory of Developmental Biology and Experimental Teratogenesis, Children's Hospital of México Federico Gomez, Mexico City 06720, Mexico.ORCID 0000-0002-0403-537X
Carlos César Patiño-MoralesResearch Laboratory of Developmental Biology and Experimental Teratogenesis, Children's Hospital of México Federico Gomez, Mexico City 06720, Mexico.ORCID 0000-0003-1995-0308
Laura Villavicencio-GuzmánResearch Laboratory of Developmental Biology and Experimental Teratogenesis, Children's Hospital of México Federico Gomez, Mexico City 06720, Mexico.ORCID 0000-0002-8314-8996
Juan Carlos CoronaLaboratory of Neurosciences, Hospital Infantil de México Federico Gómez, Mexico City 06720, Mexico.ORCID 0000-0003-4907-437X
María Cristina Revilla-MonsalveUnidad de Investigación en Enfermedades Metabólicas, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Rosa Adriana Jarillo-LunaSección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina del Instituto Politécnico Nacional, Mexico City 11340, Mexico.ORCID 0000-0003-0467-2528
Marcela Salazar-GarcíaResearch Laboratory of Developmental Biology and Experimental Teratogenesis, Children's Hospital of México Federico Gomez, Mexico City 06720, Mexico.

Funding

Fondos Federales HIM/2021/046, HIM/2019/057 and HIM/2018/046
6 · The paper itself

Abstract

Neural crest cells (NCCs) play a significant role in the development of ventricular outflow tracts (OFTs), and cardiac neural crest cells (cNCCs) are involved in the development of the embryonic conus, suggesting that these cell lineages may be a teratogenic target for the development of cardiopathies in offspring conceived under a hyperglycemic environment. We evaluate the effect of the hyperglycemic intrauterine environment on the morphological and anatomical changes in the conal ridges along with the alterations in the spatiotemporal expression of AP2α in offspring hearts at 13, 15, and 17 DPC. The anatomical and histological analysis of the hearts in the experimental group presented smaller dimensions compared to the control group in the offspring at the three ages studied. Consequently, this resulted in a hyperglycemic environment that altered the immunostaining of AP2α in the hearts of the offspring at the three ages studied. Thus, the hyperglycemic intrauterine environment in offspring caused important morphological alterations in the development of conal ridges and promoted the generation of conotruncal heart defects in which the double outlet of the right ventricle, the atrioventricular (AV) canal, predominated. Therefore, knowing that exposing the offspring to more glucose potentially can lead to complications during organogenesis of the circulatory and central nervous systems.

Indexed as

Diabetes Mellitus, ExperimentalHeartHeart Defects, CongenitalMyocardiumPrenatal Exposure Delayed EffectsTranscription Factor AP-2AnimalsFemaleGene Expression Regulation, DevelopmentalMaleNeural CrestOrganogenesisPregnancyRatsRats, WistarTranscription Factor AP-2cardiac outflow tractsconal ridgesconotruncal cardiopathiesheart developmenthyperglycemia

Identifiers

PMID40507872
PMCPMC12155284

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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.