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The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors
The raising prevalence of obesity is associated with an increased risk for cardiovascular diseases (CVDs), particularly coronary artery disease (CAD), and heart failure, including atrial fibrillation, ventricular arrhythmias and sudden death. Obesity contributes directly to incident cardiovascular r...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8868420/ https://www.ncbi.nlm.nih.gov/pubmed/35204118 http://dx.doi.org/10.3390/antiox11020235 |
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author | Gutiérrez-Cuevas, Jorge Galicia-Moreno, Marina Monroy-Ramírez, Hugo Christian Sandoval-Rodriguez, Ana García-Bañuelos, Jesús Santos, Arturo Armendariz-Borunda, Juan |
author_facet | Gutiérrez-Cuevas, Jorge Galicia-Moreno, Marina Monroy-Ramírez, Hugo Christian Sandoval-Rodriguez, Ana García-Bañuelos, Jesús Santos, Arturo Armendariz-Borunda, Juan |
author_sort | Gutiérrez-Cuevas, Jorge |
collection | PubMed |
description | The raising prevalence of obesity is associated with an increased risk for cardiovascular diseases (CVDs), particularly coronary artery disease (CAD), and heart failure, including atrial fibrillation, ventricular arrhythmias and sudden death. Obesity contributes directly to incident cardiovascular risk factors, including hyperglycemia or diabetes, dyslipidemia, and hypertension, which are involved in atherosclerosis, including structural and functional cardiac alterations, which lead to cardiac dysfunction. CVDs are the main cause of morbidity and mortality worldwide. In obesity, visceral and epicardial adipose tissue generate inflammatory cytokines and reactive oxygen species (ROS), which induce oxidative stress and contribute to the pathogenesis of CVDs. Nuclear factor erythroid 2-related factor 2 (NRF2; encoded by Nfe2l2 gene) protects against oxidative stress and electrophilic stress. NRF2 participates in the regulation of cell inflammatory responses and lipid metabolism, including the expression of over 1000 genes in the cell under normal and stressed environments. NRF2 is downregulated in diabetes, hypertension, and inflammation. Nfe2l2 knockout mice develop structural and functional cardiac alterations, and NRF2 deficiency in macrophages increases atherosclerosis. Given the endothelial and cardiac protective effects of NRF2 in experimental models, its activation using pharmacological or natural products is a promising therapeutic approach for obesity and CVDs. This review provides a comprehensive summary of the current knowledge on the role of NRF2 in obesity-associated cardiovascular risk factors. |
format | Online Article Text |
id | pubmed-8868420 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-88684202022-02-25 The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors Gutiérrez-Cuevas, Jorge Galicia-Moreno, Marina Monroy-Ramírez, Hugo Christian Sandoval-Rodriguez, Ana García-Bañuelos, Jesús Santos, Arturo Armendariz-Borunda, Juan Antioxidants (Basel) Review The raising prevalence of obesity is associated with an increased risk for cardiovascular diseases (CVDs), particularly coronary artery disease (CAD), and heart failure, including atrial fibrillation, ventricular arrhythmias and sudden death. Obesity contributes directly to incident cardiovascular risk factors, including hyperglycemia or diabetes, dyslipidemia, and hypertension, which are involved in atherosclerosis, including structural and functional cardiac alterations, which lead to cardiac dysfunction. CVDs are the main cause of morbidity and mortality worldwide. In obesity, visceral and epicardial adipose tissue generate inflammatory cytokines and reactive oxygen species (ROS), which induce oxidative stress and contribute to the pathogenesis of CVDs. Nuclear factor erythroid 2-related factor 2 (NRF2; encoded by Nfe2l2 gene) protects against oxidative stress and electrophilic stress. NRF2 participates in the regulation of cell inflammatory responses and lipid metabolism, including the expression of over 1000 genes in the cell under normal and stressed environments. NRF2 is downregulated in diabetes, hypertension, and inflammation. Nfe2l2 knockout mice develop structural and functional cardiac alterations, and NRF2 deficiency in macrophages increases atherosclerosis. Given the endothelial and cardiac protective effects of NRF2 in experimental models, its activation using pharmacological or natural products is a promising therapeutic approach for obesity and CVDs. This review provides a comprehensive summary of the current knowledge on the role of NRF2 in obesity-associated cardiovascular risk factors. MDPI 2022-01-26 /pmc/articles/PMC8868420/ /pubmed/35204118 http://dx.doi.org/10.3390/antiox11020235 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Gutiérrez-Cuevas, Jorge Galicia-Moreno, Marina Monroy-Ramírez, Hugo Christian Sandoval-Rodriguez, Ana García-Bañuelos, Jesús Santos, Arturo Armendariz-Borunda, Juan The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors |
title | The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors |
title_full | The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors |
title_fullStr | The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors |
title_full_unstemmed | The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors |
title_short | The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors |
title_sort | role of nrf2 in obesity-associated cardiovascular risk factors |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8868420/ https://www.ncbi.nlm.nih.gov/pubmed/35204118 http://dx.doi.org/10.3390/antiox11020235 |
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