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Pulmonary hypertension is a fatal lung and heart disease. It is characterized by shortness of breath, fatigue and fainting. It is exacerbated by an increase of the pressure in the lung vasculature through exercise, leading to progressive worsening of hemodynamics, right ventricular hypertrophy, right heart insufficiency and finally right heart failure. This book focuses on pulmonary arterial hypertension, a rare and progressive subgroup of pulmonary hypertension, which is today incurable and terminally faal. Classification of pulmonary arterial hypertension, its pathology, and strategies for future therapy will be of interest both to those suffering from the disease and those who take care of patients. This volume will also engage physicians and other scientists contributing to an understanding of the pathophysiology of pulmonary arterial hypertension and attempting to extend life of humans with pulmonary arterial hypertension by developing causal and curative therapies.
Pulmonary hypertension (PH) is a disorder of the pulmonary vasculature defined by increased mean pulmonary arterial pressure (mPAP) leading to right ventricle (RV) hypertrophy and dysfunction, right-sided heart failure and ultimately death. PH is a common complication of chronic lung diseases (CLD) including idiopathic pulmonary fibrosis (IPF) or chronic obstructive pulmonary disease (COPD) where it is classified as Group 3 PH by the WHO. It can also be associated with cardiovascular conditions such as left-heart disease (classified as Group 2 PH) or appear on its own as pulmonary arterial hypertension (PAH) and classified as Group1 PH. In all of these cases the diagnosis of pulmonary hypertension is strongly associated with increased morbidity and mortality. The focus of this Research Topic is to enhance our understanding of the mechanisms that contribute to the pathophysiology of pulmonary hypertension and right ventricle hypertrophy.
Oxygen sensing is a key physiological function of many tissues, but the identity of the sensor, the signalling pathways linking the sensor to the effector, and the endpoint effector mechanisms are all subjects of controversy. This book evaluates the various mediators that have been proposed, including the mitochondria, NAD(P)H oxidases, cytochrome p450 enzymes, and direct effects on enzymes and ion channels. There has been a resurgence of interest in the role of mitochondria, based partly on the ability of mitochondrial inhibitors to mimic hypoxia, but there is little consensus concerning mechanisms. Some favour the view that the primary signalling event is a reduction in cell redox state an...
This Research Topic assembles original contributions and reviews from an international consortium of PIs related to interactions between pro-inflammatory cytokines and ion channels during acute lung injury and chronic heart failure.
The American Heart Association’s Scientific Sessions 2019 is bringing big science, big technology, and big networking opportunities to Philadelphia, Pennsylvania this November. This event features five days of the best in science and cardiovascular clinical practice covering all aspects of basic, clinical, population and translational content.
The main goal of this book is to form a high-quality platform in which well-known and emerging pioneering basic, translational and clinical scientists can present their latest, exciting findings in the studies of redox signaling in the pulmonary vasculature. Content from outstanding investigators with unique expertise and skills of molecular and cell biology, biochemistry, physiology, pharmacology, biophysics, biotechnology and medicine will update our current out-of-date concepts with new knowledge. Rapidly increasing scientific studies have gathered a large volume of novel and important information on redox signaling in healthy and diseased pulmonary vasculature. This volume covers the nee...