Reactive oxygen species (ROS), nitric oxide and other reactive nitrogen species (RNS), are produced by the cells of the cardiovascular system. Oxidative and nitrosative stress may induce damage leading to a variety of diseases, but controlled ROS/RNS generation play a role in redox-sensitive gene expression and cell signaling regulating a plethora of physiological processes.
Redox and nitrosative signaling is involved in the control of a large number of vascular functions. Among them the regulation of the vascular tone by the endothelium and smooth muscle cells or the control of blood pressure. Also cardiac functions such as excitation-contraction coupling or myocyte force development are redox signaling-dependent events. Of note, during exercise bursts of ROS and RNS are produced by the cells of the cardiovascular system, which seem essential for the induction of beneficial effects of training. However, ROS/RNS may have damaging effects in various cardiac and vascular disorders such as coronary heart disease, ventricular hypertrophy, cardiac arrhythmias and heart failure, to name only a few.
Since the discovery of the physiological role of ROS in cell signaling the number of papers in this filed has grown exponentially and great advances in the knowledge have been achieved. However, many issues of ROS biology in cardiovascular system remain to be elucidated, including the vascular tissue specific sources and targets of ROS, or the mechanisms underlying the fine tuning of ROS levels delimiting the boundary between physiological and pathological vascular events. Also a field in great expansion is the redox-dependent epigenetic regulation of vascular gene expression and the interplay between redox signaling and DNA oxidation based on the redox regulation of DNA damage repair proteins.
In this Research Topic, we welcome papers evaluating the role of redox and nitrosative signaling in cardiac and vascular functions as well as in the pathogenesis of cardiovascular diseases related to the disruption of ROS/RNS homeostasis and oxidative and nitrosative stress.
To reach a broad audience of scientists working in the field of redox biomedicine, we encourage the submission of papers approaching the topic from different points of view and at different levels, from basic to translational research. While oxidant-scavenging therapies have been disappointing, new insights into oxidative/nitrosative stress are paving the way for a very different approach. Therefore, the role of endogenous and exogenous antioxidants and their putative role in cardiovascular protection could be considered. A collection of scientific reports with different approaches can contribute to highlight these interesting aspects of cardiovascular biology with a unified vision that can contribute to the development of new ideas and advancements in the field of redox and nitrosative signaling in the control of normal cardiovascular functions and their disruption in diseases.
Reactive oxygen species (ROS), nitric oxide and other reactive nitrogen species (RNS), are produced by the cells of the cardiovascular system. Oxidative and nitrosative stress may induce damage leading to a variety of diseases, but controlled ROS/RNS generation play a role in redox-sensitive gene expression and cell signaling regulating a plethora of physiological processes.
Redox and nitrosative signaling is involved in the control of a large number of vascular functions. Among them the regulation of the vascular tone by the endothelium and smooth muscle cells or the control of blood pressure. Also cardiac functions such as excitation-contraction coupling or myocyte force development are redox signaling-dependent events. Of note, during exercise bursts of ROS and RNS are produced by the cells of the cardiovascular system, which seem essential for the induction of beneficial effects of training. However, ROS/RNS may have damaging effects in various cardiac and vascular disorders such as coronary heart disease, ventricular hypertrophy, cardiac arrhythmias and heart failure, to name only a few.
Since the discovery of the physiological role of ROS in cell signaling the number of papers in this filed has grown exponentially and great advances in the knowledge have been achieved. However, many issues of ROS biology in cardiovascular system remain to be elucidated, including the vascular tissue specific sources and targets of ROS, or the mechanisms underlying the fine tuning of ROS levels delimiting the boundary between physiological and pathological vascular events. Also a field in great expansion is the redox-dependent epigenetic regulation of vascular gene expression and the interplay between redox signaling and DNA oxidation based on the redox regulation of DNA damage repair proteins.
In this Research Topic, we welcome papers evaluating the role of redox and nitrosative signaling in cardiac and vascular functions as well as in the pathogenesis of cardiovascular diseases related to the disruption of ROS/RNS homeostasis and oxidative and nitrosative stress.
To reach a broad audience of scientists working in the field of redox biomedicine, we encourage the submission of papers approaching the topic from different points of view and at different levels, from basic to translational research. While oxidant-scavenging therapies have been disappointing, new insights into oxidative/nitrosative stress are paving the way for a very different approach. Therefore, the role of endogenous and exogenous antioxidants and their putative role in cardiovascular protection could be considered. A collection of scientific reports with different approaches can contribute to highlight these interesting aspects of cardiovascular biology with a unified vision that can contribute to the development of new ideas and advancements in the field of redox and nitrosative signaling in the control of normal cardiovascular functions and their disruption in diseases.
