About this Research Topic
This Research Topic is the second volume of the 'Oxidative Stress in Cardiovascular Diseases and Pulmonary Hypertension.' Please find the first volume here.
Cardiovascular and pulmonary vascular disease are the leading cause for morbidity and mortality worldwide. To tackle these, improvement in our understanding about the pathophysiology and current status of treatment for heart and lung diseases are extremely necessary. Oxidative stress has been considered as a major hall mark involved for the pathogenesis and development in heart and lung disorders, including cardiovascular diseases and pulmonary hypertension. In this line, tissue and cell specific reactive oxygen or nitrogen species (ROS/RNS) are regarded as major important elements in physiological and pathophysiological enzymatic processes for the regulation of growth, apoptosis, and maintenance of various signaling cascades including cellular homeostasis, cellular metabolism and immune function. However, if there is any imbalance in the formation of ROS/RNS radicals such as superoxide anions, hydroxyl radicals, hydrogen peroxide, nitric oxide and peroxynitrite, this may cause oxidative stress to mediate endothelial dysfunction, activate inflammations and impair vascular structure tone and functions. The pathological increase of ROS/RNS may mediate DNA/RNA damage, lipid peroxidation, protein oxidation/nitration and other cellular/systemic compromised conditions. ROS is produced from cellular or mitochondrial NADPH oxidases, xanthine oxidase, uncoupled endothelial nitric oxide synthase and RNS inducible nitric oxide synthase is generated from nitric oxide syntheses. Experimental evidence supports that ROS/RNS play very important roles in cardiovascular and pulmonary diseases. However, it is still not clear how ROS/RNS play differently in vascular and tissue specific form. In this line, this Research Topic will demonstrate to the reader the current understanding about the role of ROS/RNS in the pathophysiology of cardiovascular/pulmonary hypertension diseases.
Cardiovascular and respiratory diseases are the leading causes of death worldwide. Experimental evidences suggesting that the imbalance of oxidative stress has a crucial role for the manifestation of this disease. This article collection will try to highlight current understanding and progress about the role of ROS/RNS in cardiovascular diseases including pulmonary hypertension.
In this Research Topic, we invite researchers to provide original research or review articles that will help to under-stand the role of oxidative/nitrosative stress in cardiovascular diseases and pulmonary hypertension. We also en-courage authors to submit articles on the study following their source with particular emphasis on cellular and molecular mechanism as well as the potential therapeutic effects against oxidative stress in cardiovascular diseases including pulmonary hypertension.
Further, our collection will cover the following areas:
1) Effects of reactive oxygen or nitrogen species (ROS/ RNS) mediated signal transduction in cardiovascular diseases including pulmonary hypertension.
2) Role of tissue/vascular specific RNS/ROS in protein kinases A and G in cardiovascular diseases including pulmonary hypertension.
3) ROS/RNS mediated effect on protein quality control in cardiovascular diseases including pulmonary hypertension.
4) ROS/RNS mediated role on post-translational modification of regulated proteins in cardiovascular diseases including pulmonary hypertension.
5) Roles of oxidative stress and/or inflammation in onset and development of heart failure/pulmonary hypertension.
6) Oxidative stress mediated effect on structure and function of cellular mitochondria; cardiomyocyte, vascular smooth muscle cells, pulmonary vascular wall remodeling etc.
7) Understanding the cellular source of ROS/RNS mediated oxidative stress that is involved in cellular and molecular mechanisms in cardiovascular/pulmonary biology.
8) Experimental studies using animal and cell culture models to mediate the role of ROS/RNS/oxidative stress in cardiovascular diseases including pulmonary hypertension.
9) Oxidative stress mediated epigenetic modification in cardiovascular diseases including pulmonary hypertension.
10) Biomarkers of oxidative stress and inflammation in cardiovascular diseases including pulmonary hypertension.
11) Any therapeutic role of antioxidant/anti-inflammatory treatment in cardiovascular diseases including pulmonary hypertension.
12) Oxidative stress mediated effect on transcription factors in cardiovascular diseases including pulmonary hypertension.
13) Any metabolic role of ROS/RNS in cardiovascular diseases including pulmonary hypertension.
Cardiovascular and pulmonary vascular disease are the leading cause for morbidity and mortality worldwide. To tackle these, improvement in our understanding about the pathophysiology and current status of treatment for heart and lung diseases are extremely necessary. Oxidative stress has been considered as a major hall mark involved for the pathogenesis and development in heart and lung disorders, including cardiovascular diseases and pulmonary hypertension. In this line, tissue and cell specific reactive oxygen or nitrogen species (ROS/RNS) are regarded as major important elements in physiological and pathophysiological enzymatic processes for the regulation of growth, apoptosis, and maintenance of various signaling cascades including cellular homeostasis, cellular metabolism and immune function. However, if there is any imbalance in the formation of ROS/RNS radicals such as superoxide anions, hydroxyl radicals, hydrogen peroxide, nitric oxide and peroxynitrite, this may cause oxidative stress to mediate endothelial dysfunction, activate inflammations and impair vascular structure tone and functions. The pathological increase of ROS/RNS may mediate DNA/RNA damage, lipid peroxidation, protein oxidation/nitration and other cellular/systemic compromised conditions. ROS is produced from cellular or mitochondrial NADPH oxidases, xanthine oxidase, uncoupled endothelial nitric oxide synthase and RNS inducible nitric oxide synthase is generated from nitric oxide syntheses. Experimental evidence supports that ROS/RNS play very important roles in cardiovascular and pulmonary diseases. However, it is still not clear how ROS/RNS play differently in vascular and tissue specific form. In this line, this Research Topic will demonstrate to the reader the current understanding about the role of ROS/RNS in the pathophysiology of cardiovascular/pulmonary hypertension diseases.
Cardiovascular and respiratory diseases are the leading causes of death worldwide. Experimental evidences suggesting that the imbalance of oxidative stress has a crucial role for the manifestation of this disease. This article collection will try to highlight current understanding and progress about the role of ROS/RNS in cardiovascular diseases including pulmonary hypertension.
In this Research Topic, we invite researchers to provide original research or review articles that will help to under-stand the role of oxidative/nitrosative stress in cardiovascular diseases and pulmonary hypertension. We also en-courage authors to submit articles on the study following their source with particular emphasis on cellular and molecular mechanism as well as the potential therapeutic effects against oxidative stress in cardiovascular diseases including pulmonary hypertension.
Further, our collection will cover the following areas:
1) Effects of reactive oxygen or nitrogen species (ROS/ RNS) mediated signal transduction in cardiovascular diseases including pulmonary hypertension.
2) Role of tissue/vascular specific RNS/ROS in protein kinases A and G in cardiovascular diseases including pulmonary hypertension.
3) ROS/RNS mediated effect on protein quality control in cardiovascular diseases including pulmonary hypertension.
4) ROS/RNS mediated role on post-translational modification of regulated proteins in cardiovascular diseases including pulmonary hypertension.
5) Roles of oxidative stress and/or inflammation in onset and development of heart failure/pulmonary hypertension.
6) Oxidative stress mediated effect on structure and function of cellular mitochondria; cardiomyocyte, vascular smooth muscle cells, pulmonary vascular wall remodeling etc.
7) Understanding the cellular source of ROS/RNS mediated oxidative stress that is involved in cellular and molecular mechanisms in cardiovascular/pulmonary biology.
8) Experimental studies using animal and cell culture models to mediate the role of ROS/RNS/oxidative stress in cardiovascular diseases including pulmonary hypertension.
9) Oxidative stress mediated epigenetic modification in cardiovascular diseases including pulmonary hypertension.
10) Biomarkers of oxidative stress and inflammation in cardiovascular diseases including pulmonary hypertension.
11) Any therapeutic role of antioxidant/anti-inflammatory treatment in cardiovascular diseases including pulmonary hypertension.
12) Oxidative stress mediated effect on transcription factors in cardiovascular diseases including pulmonary hypertension.
13) Any metabolic role of ROS/RNS in cardiovascular diseases including pulmonary hypertension.
Keywords: Cardiovascular, Pulmonary hypertension, Oxidative stress, Reactive oxygen species, Reactive nitrogen species, NADPH oxidases, Nitric oxide synthase
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