Cardiovascular diseases (CVDs) constitute the leading causes of death and reduced quality of life worldwide. Reactive oxygen species (ROS) and various immune cells participate in crucial signalling pathways implicated in the homeostasis of the cardiovascular system. Therefore, excessive ROS production can affect various immune cells leading to their metabolic reprogramming intertwined with activation, proliferation, and cytokine production. Furthermore, redox post-translational protein modification may enhance neoantigens formation, which regulates antigen presentation, inflammasome activation and T-cell immunity. Enhanced immune system activation has been widely demonstrated to lead to vascular, kidney and cardiac cell injury and, consequently, target-organ damage associated with CVDs, such as vascular dysfunction, atherogenesis or heart and kidney failure. Furthermore, oxidative stress and inflammation are closely interrelated, which may perpetuate a vicious oxidative stress-inflammatory loop and the progression of pathology.
Enhanced production of ROS and chronic inflammation have been considered risk factors for developing CVDs. Some oxidative stress and inflammatory markers are enhanced in CVDs and harbour prognostic implications. For all these reasons, antioxidants or anti-inflammatory drugs may represent promising therapies. Nevertheless, only a few clinical trials targeting ROS and inflammatory mediators demonstrated the beneficial effects of such targeting due to the pleiotropic effect of antioxidant and anti-inflammatory drugs. This highlights the complexity of redox and immune systems and indicates that other approaches are essential to assess the value of therapeutic modulation of ROS and inflammation in CVDs.
This research article collection aims to provide insight into the pathophysiological role of ROS in redox post-translational modification, metabolic reprogramming and activation of innate and adaptive immune cells and their mutual interaction as factors leading to the development of CVDs and target organ damage. Understanding novel molecular pathways leading to metabolic reprogramming of the immune cells mediated by chronic oxidative stress is essential for understanding the pathology of CVDs. Moreover, it will enable the future discovery of novel integrative therapeutic approaches targeting CVDs.
This Article Collection will focus on the role of oxidative stress, immune cells, chronic inflammation and their mutual interaction as factors leading to CVDs. We are looking for high-quality basic and clinical research articles related to the following themes:
- The role of reactive oxygen species in metabolic reprogramming and activation of innate and adaptive immune cells in CVDs;
- The impact of redox post-translational protein modification in immune cell activation in CVDs;
- Crosstalk between NADPH oxidase (NOX)-mediated and mitochondrial-derived reactive oxygen species and immune cells in the vasculature, heart, brain and kidney;
- Novel genetic or molecular markers, pathways and mechanisms leading to inflammation and oxidative stress in CVDs;
- Inflammation and oxidative stress as targets for novel therapeutic approaches;
- Clinical translational research targeting ROS production and inflammation in CVDs.
We are happy to consider submissions on CVDs including, but not limited to, hypertension, atherosclerosis, heart failure, stroke, chronic kidney disease or aortic aneurysm. Finally, comprehensive review articles addressing the association and interaction between oxidative stress and immune cells in CVDs will also be welcome.
Cardiovascular diseases (CVDs) constitute the leading causes of death and reduced quality of life worldwide. Reactive oxygen species (ROS) and various immune cells participate in crucial signalling pathways implicated in the homeostasis of the cardiovascular system. Therefore, excessive ROS production can affect various immune cells leading to their metabolic reprogramming intertwined with activation, proliferation, and cytokine production. Furthermore, redox post-translational protein modification may enhance neoantigens formation, which regulates antigen presentation, inflammasome activation and T-cell immunity. Enhanced immune system activation has been widely demonstrated to lead to vascular, kidney and cardiac cell injury and, consequently, target-organ damage associated with CVDs, such as vascular dysfunction, atherogenesis or heart and kidney failure. Furthermore, oxidative stress and inflammation are closely interrelated, which may perpetuate a vicious oxidative stress-inflammatory loop and the progression of pathology.
Enhanced production of ROS and chronic inflammation have been considered risk factors for developing CVDs. Some oxidative stress and inflammatory markers are enhanced in CVDs and harbour prognostic implications. For all these reasons, antioxidants or anti-inflammatory drugs may represent promising therapies. Nevertheless, only a few clinical trials targeting ROS and inflammatory mediators demonstrated the beneficial effects of such targeting due to the pleiotropic effect of antioxidant and anti-inflammatory drugs. This highlights the complexity of redox and immune systems and indicates that other approaches are essential to assess the value of therapeutic modulation of ROS and inflammation in CVDs.
This research article collection aims to provide insight into the pathophysiological role of ROS in redox post-translational modification, metabolic reprogramming and activation of innate and adaptive immune cells and their mutual interaction as factors leading to the development of CVDs and target organ damage. Understanding novel molecular pathways leading to metabolic reprogramming of the immune cells mediated by chronic oxidative stress is essential for understanding the pathology of CVDs. Moreover, it will enable the future discovery of novel integrative therapeutic approaches targeting CVDs.
This Article Collection will focus on the role of oxidative stress, immune cells, chronic inflammation and their mutual interaction as factors leading to CVDs. We are looking for high-quality basic and clinical research articles related to the following themes:
- The role of reactive oxygen species in metabolic reprogramming and activation of innate and adaptive immune cells in CVDs;
- The impact of redox post-translational protein modification in immune cell activation in CVDs;
- Crosstalk between NADPH oxidase (NOX)-mediated and mitochondrial-derived reactive oxygen species and immune cells in the vasculature, heart, brain and kidney;
- Novel genetic or molecular markers, pathways and mechanisms leading to inflammation and oxidative stress in CVDs;
- Inflammation and oxidative stress as targets for novel therapeutic approaches;
- Clinical translational research targeting ROS production and inflammation in CVDs.
We are happy to consider submissions on CVDs including, but not limited to, hypertension, atherosclerosis, heart failure, stroke, chronic kidney disease or aortic aneurysm. Finally, comprehensive review articles addressing the association and interaction between oxidative stress and immune cells in CVDs will also be welcome.
