Endothelial NOX5 overexpression induces changes in the cardiac gene profile: potential impact in myocardial infarction?
Keywords: 
Oxidative stress
NOX5
Myocardial infarction
Echocardiography
Issue Date: 
2023
Publisher: 
Springer
Project: 
info:eu-repo/grantAgreement/MINECO/Retos Investigación: Proyectos de I+D+I/SAF2013-49088-R/[ES]/NUEVOS MECANISMOS DE ESTRES OXIDATIVO EN LA FISIOPATOLOGIA VASCULAR: PAPEL DE LA NADPH OXIDASA 5
ISSN: 
1877-8755
37566320
Note: 
This article is licensed under a Creative Commons Attribution 4.0 International License
Citation: 
Cortés, A. (Adriana); Marqués, J. (Javier); Pejenaute-Martínez-de-Lizarrondo, Á. (Álvaro); et al. "Endothelial NOX5 overexpression induces changes in the cardiac gene profile: potential impact in myocardial infarction?". Journal of Physiology and Biochemistry. 79, 2023, 787 - 797
Abstract
Cardiovascular diseases and the ischemic heart disease specifically constitute the main cause of death worldwide. The ischemic heart disease may lead to myocardial infarction, which in turn triggers numerous mechanisms and pathways involved in cardiac repair and remodeling. Our goal in the present study was to characterize the effect of the NADPH oxidase 5 (NOX5) endothelial expression in healthy and infarcted knock-in mice on diverse signaling pathways. The mechanisms studied in the heart of mice were the redox pathway, metalloproteinases and collagen pathway, signaling factors such as NFκB, AKT or Bcl-2, and adhesion molecules among others. Recent studies support that NOX5 expression in animal models can modify the environment and predisposes organ response to harmful stimuli prior to pathological processes. We found many alterations in the mRNA expression of components involved in cardiac fibrosis as collagen type I or TGF-β and in key players of cardiac apoptosis such as AKT, Bcl-2, or p53. In the heart of NOX5-expressing mice after chronic myocardial infarction, gene alterations were predominant in the redox pathway (NOX2, NOX4, p22phox, or SOD1), but we also found alterations in VCAM-1 and β-MHC expression. Our results suggest that NOX5 endothelial expression in mice preconditions the heart, and we propose that NOX5 has a cardioprotective role. The correlation studies performed between echocardiographic parameters and cardiac mRNA expression supported NOX5 protective action.

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