Related Experiment Video
Updated: Jul 19, 2025
En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Endothelial NOX5 overexpression induces changes in the cardiac gene profile: potential impact in myocardial
Adriana Cortés1,2, Javier Marqués1,2, Álvaro Pejenaute1,2
1Department of Biochemistry and Genetics, University of Navarra, Pamplona, Spain.
Insights
NADPH oxidase 5 (NOX5) endothelial expression in mice preconditions the heart, suggesting a cardioprotective role. This finding is crucial for understanding heart repair after myocardial infarction and developing new therapeutic strategies.
Area of Science:
- Cardiovascular research
- Molecular biology
- Physiology
Background:
- Cardiovascular diseases, particularly ischemic heart disease, are leading global causes of mortality.
- Myocardial infarction initiates complex cardiac repair and remodeling processes.
- NADPH oxidase 5 (NOX5) expression's role in cardiac response to injury is not fully understood.
Purpose of the Study:
- To investigate the impact of endothelial NOX5 expression on signaling pathways in healthy and infarcted mouse hearts.
- To characterize NOX5's influence on redox, fibrosis, apoptosis, and adhesion molecule pathways post-myocardial infarction.
Main Methods:
- Utilized knock-in mouse models with varying NOX5 expression.
- Analyzed cardiac mRNA expression related to redox, metalloproteinases, collagen, apoptosis, and adhesion molecules.
- Correlated echocardiographic parameters with cardiac mRNA expression.
Main Results:
- Found significant alterations in mRNA expression of cardiac fibrosis (collagen type I, TGF-β) and apoptosis (AKT, Bcl-2, p53) markers.
- Observed predominant changes in the redox pathway (NOX2, NOX4, p22phox, SOD1) in NOX5-expressing mice post-infarction.
- Detected alterations in VCAM-1 and β-MHC expression, alongside evidence supporting NOX5's protective action.
Conclusions:
- Endothelial NOX5 expression in mice appears to precondition the heart, suggesting a cardioprotective role.
- NOX5 may modulate key pathways involved in cardiac response to chronic myocardial infarction.
- Further research into NOX5's mechanisms could offer novel therapeutic avenues for ischemic heart disease.
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.
Related Concept Videos
01:21Myocarditis I: Introduction
01:26Coronary Artery Disease II: Pathophysiology
01:28Nitric Oxide Signaling Pathway
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
01:29Pathophysiology of Cardiac Performance
01:29Cardiomyopathy III: Hypertrophic Cardiomyopathy