Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies

Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a...

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Autores principales:	Bart De Geest, Mudit Mishra
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	gene therapy gene transfer heart failure oxidative stress reactive oxygen species cardiac hypertrophy Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/1b751689f64640ada787345a6657449f
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spelling	oai:doaj.org-article:1b751689f64640ada787345a6657449f2021-11-25T16:50:05ZRole of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies10.3390/biomedicines91116452227-9059https://doaj.org/article/1b751689f64640ada787345a6657449f2021-11-01T00:00:00Zhttps://www.mdpi.com/2227-9059/9/11/1645https://doaj.org/toc/2227-9059Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a persistent increase of steady-state ROS levels leading to disturbed signaling pathways and oxidative modification of cellular constituents. It is a key pathophysiological player in pathological hypertrophy, pathological remodeling, and the development and progression of heart failure. The heart is the metabolically most active organ and is characterized by the highest content of mitochondria of any tissue. Mitochondria are the main source of ROS in the myocardium. The causal role of oxidative stress in heart failure is highlighted by gene transfer studies of three primary antioxidant enzymes, thioredoxin, and heme oxygenase-1, and is further supported by gene therapy studies directed at correcting oxidative stress linked to metabolic risk factors. Moreover, gene transfer studies have demonstrated that redox-sensitive microRNAs constitute potential therapeutic targets for the treatment of heart failure. In conclusion, gene therapy studies have provided strong corroborative evidence for a key role of oxidative stress in pathological remodeling and in the development of heart failure.Bart De GeestMudit MishraMDPI AGarticlegene therapygene transferheart failureoxidative stressreactive oxygen speciescardiac hypertrophyBiology (General)QH301-705.5ENBiomedicines, Vol 9, Iss 1645, p 1645 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	gene therapy gene transfer heart failure oxidative stress reactive oxygen species cardiac hypertrophy Biology (General) QH301-705.5
spellingShingle	gene therapy gene transfer heart failure oxidative stress reactive oxygen species cardiac hypertrophy Biology (General) QH301-705.5 Bart De Geest Mudit Mishra Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies
description	Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a persistent increase of steady-state ROS levels leading to disturbed signaling pathways and oxidative modification of cellular constituents. It is a key pathophysiological player in pathological hypertrophy, pathological remodeling, and the development and progression of heart failure. The heart is the metabolically most active organ and is characterized by the highest content of mitochondria of any tissue. Mitochondria are the main source of ROS in the myocardium. The causal role of oxidative stress in heart failure is highlighted by gene transfer studies of three primary antioxidant enzymes, thioredoxin, and heme oxygenase-1, and is further supported by gene therapy studies directed at correcting oxidative stress linked to metabolic risk factors. Moreover, gene transfer studies have demonstrated that redox-sensitive microRNAs constitute potential therapeutic targets for the treatment of heart failure. In conclusion, gene therapy studies have provided strong corroborative evidence for a key role of oxidative stress in pathological remodeling and in the development of heart failure.
format	article
author	Bart De Geest Mudit Mishra
author_facet	Bart De Geest Mudit Mishra
author_sort	Bart De Geest
title	Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies
title_short	Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies
title_full	Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies
title_fullStr	Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies
title_full_unstemmed	Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies
title_sort	role of oxidative stress in heart failure: insights from gene transfer studies
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/1b751689f64640ada787345a6657449f
work_keys_str_mv	AT bartdegeest roleofoxidativestressinheartfailureinsightsfromgenetransferstudies AT muditmishra roleofoxidativestressinheartfailureinsightsfromgenetransferstudies
_version_	1718412880413458432

Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies

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