Lung Inflammation in Health and Disease, Volume I

Respiratory diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma, the most common chronic disease. Each year, tens of millions of people develop and can die from from respiratory infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for those affected.
Current treatment options for lung disease are neither effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses.
This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinicalresearch, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.

Presents state-of-the-art research and clinical tools in one collection for the first time Designed to inspire the development of novel therapeutics and technology Critical resource providing researchers, clinicians, professionals, fellows, and students a deeper understanding of the underlying causes and effects of lung inflammation in health and disease

Autorentext

Dr. Yong-Xiao Wang is a Full Professor in the Department of Molecular and Cellular Physiology at Albany Medical College, Albany, New York, USA. He received his M.D. at the Wannan Medical College (China), Ph.D. at the Fourth Military Medical University (China), and postdoctoral training at the Technical University of Munich (Germany) as well as the University of Pennsylvania (USA). Dr. Wang's primary research interests have focused on basic, translational, and drug discovery research concerning cardiac arrhythmias and hypertrophy, pulmonary hypertension, asthma, and diabetes for over 30 years. In particular, he has had extensive research experience in the studies of the molecular geneses, regulatory mechanisms, network pathways, physiological functions, and the critical roles of calcium, redox, inflammatory, and other signaling in the aforementioned illnesses. Dr. Wang has been the corresponding author, first author, and key contributor in numerous publications in highly peer-reviewed journals including Nat Commun, Antioxid Redox Signal, Proc Natl Acad Sci USA, Free Radic Biol Med, Cell Calcium, J Gen Physiol, J Biol Chem, FASEB J, Nature, Circ Res, and more. He has been the editor of several academic books in the field including a recent one entitled "Pulmonary Vasculature Redox Signaling in Health and Disease" that was published by Springer International Publishing AG in 2017. Dr. Wang has been the principal investigator on multiple research grants and awards from the National Institutes of Health, American Heart Association, American Diabetes Association, and other agencies. He has collaborated with numerous well-known scientists, served on various grant review panels, been the Editor-In-Chief and Editorial Board Member for several scientific journals, and trained a number of scholars, some of whom have become well-known independent investigators in the field.

Inhalt

1. Potential role of mast cells in regulating corticosteroid insensitivity in severe asthma.- 2. Galectin-3 Promotes ROS, Inflammation and Vascular Fibrosis in Pulmonary Arterial Hypertension.- 3. Anti-Inflammatory Effects of Statins in Lung Vascular Pathology: From Basic Science to Clinical Trials.- 4. Evolving Schema for Employing Network Biology Approaches to Understand Pulmonary Hypertension.- 5. Pulmonary Inflammation and KRAS Mutation in Lung Cancer.- 6. microRNA Targets for Asthma Therapy.- 7. Roles of genetic predisposition in the sex-bias of pulmonary pathophysiology, as a function of estrogens.- 8. Hypercapnic respiratory failure-driven skeletal muscle dysfunction: It is time for animal mod-els-based mechanistic research.- 9. Role of airway smooth muscle in inflammation related to asthma and COPD.- 10. Systemic Sclerosis and Pulmonary Disease.- 11. Innate Lymphoid Cells in airway inflammation.- 12. Sjogren's Syndrome and pulmonary disease.- 13. Redox Regulation, Oxidative Stress and Inflammation in Group 3 Pulmonary Hypertension.- 14. Sex-Steroid Signaling in Lung Diseases and Inflammation.- 15. Cytokines, Chemokines and Inflammation in Pulmonary Arterial Hypertension.- 16. Interactive roles of CaMKII/Ryanodine Receptor Signaling and Inflammation in Lung Diseases.- 17. Reciprocal Correlations of Inflammatory and Calcium Signaling in Asthma Pathogenesis.- 18. Crosstalk between Lung and Extrapulmonary Organs in Infection and Inflammation.- 19. Inflammation in Pulmonary Arterial Hypertension.- 20. Lysophospholids in Lung Inflammatory Diseases. <p