Endogenous oxidants (e.g., from mitochondrial electron transport during respiration or during phagocyte activation) and exogenous oxidants (e.g., from air pollution or cigarette smoke) are constantly present in biological systems. Reactive oxygen species (ROS) are highly unstable entities that can initiate oxidation due to their unpaired electrons. ROS are second messengers that are produced as a by-product of regular cellular metabolism. ROS help to maintain cellular redox equilibrium in order to protect cells from oxidative damage under physiological settings. Excessive stimulation of decreased nicotinamide adenine dinucleotide phosphate by cytokines, mitochondrial electron transport chain or xanthine oxidase by cytokines causes oxidative stress. Oxidative stress is a harmful process that causes lung damage and, as a result, a variety of diseases. The ability to manipulate antioxidants pharmacologically in the treatment of lung inflammation and injury could be aided by understanding the processes of ROS regulation.
Oxidative stress is now implicated in lung disorders such as asthma, COPD, ALI, pulmonary fibrosis, and lung cancer, according to a growing body of research. Through the activation of redox sensitive transcription factors and thus proinflammatory gene expression, oxidative stress plays a significant role in inflammatory responses in lung disorders. Oxidative stress is caused by inflammation in the lungs. ROS appear to be important regulatory factors in the molecular processes that lead to lung disease induction, and they may be targets for therapeutic intervention. COVID-19, like many other respiratory viral infections, causes infected cells to die, activate the innate immune system, and secrete inflammatory cytokines. All of these processes are linked to the onset of oxidative stress, which plays a significant role in the pathogenesis of viral infections. Furthermore, understanding the molecular mechanisms of ROS-mediated pathophysiological processes and how antioxidants inhibit them may aid in the development of innovative therapeutics that target the corresponding molecular pathways.
We hope that by publishing this Research Topic, we will be able to collect both experimental data that clarifies mechanisms and clinical research, such as interventional or observational studies, that will inspire fundamental researchers to come up with new research subjects. The following subjects are welcome in this special issue but not an exhaustive list:
• ROS chemistry and biochemistry, as well as free radical generation sources
• Signalling mechanisms activated by reactive oxygen species (ROS)
• Oxidative stress in lung diseases: mechanisms and effects
• The function of reactive oxygen species (ROS) in the pathogenesis of lung disorders such as asthma, COPD, ALI, pulmonary fibrosis, and lung cancer, as well as the role of antioxidants.
• Current clinical practise with oxidative stress indicators in infectious respiratory disorders
• COVID-19 and Oxidative Stress
Endogenous oxidants (e.g., from mitochondrial electron transport during respiration or during phagocyte activation) and exogenous oxidants (e.g., from air pollution or cigarette smoke) are constantly present in biological systems. Reactive oxygen species (ROS) are highly unstable entities that can initiate oxidation due to their unpaired electrons. ROS are second messengers that are produced as a by-product of regular cellular metabolism. ROS help to maintain cellular redox equilibrium in order to protect cells from oxidative damage under physiological settings. Excessive stimulation of decreased nicotinamide adenine dinucleotide phosphate by cytokines, mitochondrial electron transport chain or xanthine oxidase by cytokines causes oxidative stress. Oxidative stress is a harmful process that causes lung damage and, as a result, a variety of diseases. The ability to manipulate antioxidants pharmacologically in the treatment of lung inflammation and injury could be aided by understanding the processes of ROS regulation.
Oxidative stress is now implicated in lung disorders such as asthma, COPD, ALI, pulmonary fibrosis, and lung cancer, according to a growing body of research. Through the activation of redox sensitive transcription factors and thus proinflammatory gene expression, oxidative stress plays a significant role in inflammatory responses in lung disorders. Oxidative stress is caused by inflammation in the lungs. ROS appear to be important regulatory factors in the molecular processes that lead to lung disease induction, and they may be targets for therapeutic intervention. COVID-19, like many other respiratory viral infections, causes infected cells to die, activate the innate immune system, and secrete inflammatory cytokines. All of these processes are linked to the onset of oxidative stress, which plays a significant role in the pathogenesis of viral infections. Furthermore, understanding the molecular mechanisms of ROS-mediated pathophysiological processes and how antioxidants inhibit them may aid in the development of innovative therapeutics that target the corresponding molecular pathways.
We hope that by publishing this Research Topic, we will be able to collect both experimental data that clarifies mechanisms and clinical research, such as interventional or observational studies, that will inspire fundamental researchers to come up with new research subjects. The following subjects are welcome in this special issue but not an exhaustive list:
• ROS chemistry and biochemistry, as well as free radical generation sources
• Signalling mechanisms activated by reactive oxygen species (ROS)
• Oxidative stress in lung diseases: mechanisms and effects
• The function of reactive oxygen species (ROS) in the pathogenesis of lung disorders such as asthma, COPD, ALI, pulmonary fibrosis, and lung cancer, as well as the role of antioxidants.
• Current clinical practise with oxidative stress indicators in infectious respiratory disorders
• COVID-19 and Oxidative Stress
