Pulmonary vasculature redox signaling in health and disease

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 wi...

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Bibliographic Details
Other Authors Wang, Yong-Xiao (Editor)
Format Electronic eBook
LanguageEnglish
Published Cham, Switzerland : Springer, 2017.
SeriesAdvances in experimental medicine and biology ; v. 967.
Subjects
Active oxygen > Physiological effect.
Oxidation, Physiological.
elektronické knihy
electronic books
Online AccessFull text
ISBN9783319632452
9783319632445
ISSN0065-2598 ;
Physical Description1 online resource (xxi, 422 pages) : illustrations (some color)

Cover

Table of Contents:
  • Preface
  • About the Editor
  • Contents
  • Contributors
  • Adventitial Fibroblast Nox4 Expression and ROS Signaling in Pulmonary Arterial Hypertension
  • 1 Pulmonary Arterial Hypertension
  • 2 Reactive Oxygen Species, NADPH Oxidase and PAH
  • 3 Nox4 Expression in PAH
  • 4 Enzymatic Properties of Nox4
  • 5 Role of the Adventitial Fibroblast and Nox4 in PAH
  • References
  • Role of Transcription Factors in Pulmonary Artery Smooth Muscle Cells: An Important Link to Hypoxic Pulmonary Hypertension
  • 1 Introduction
  • 2 Roles of Transcription Factors in Lung Diseases2.1 NF-ÎðB
  • 2.2 AP-1
  • 2.3 STAT
  • 2.4 TCF7
  • 2.5 NRF2
  • 2.6 HIF-1
  • 3 Redox-Sensitive Signaling in SMC Regulation: Role of TFs
  • 4 Conclusion and Future Perspective
  • References
  • Molecular Basis of Nitrative Stress in the Pathogenesis of Pulmonary Hypertension
  • 1 Introduction
  • 2 Molecular Mechanisms of Nitrative Stress in the Pathogenesis of Pulmonary Hypertension
  • 3 Molecular Sources of Reactive Nitrogen Species in Pulmonary Hypertension
  • 4 Molecular Sources of Reactive Oxygen Species in Pulmonary Hypertension5 Nitrative Stress in Pulmonary Hypertension Patients
  • 6 Conclusions
  • References
  • Pentose Shunt, Glucose-6-ÂƯPhosphate Dehydrogenase, NADPH Redox, and Stem Cells in Pulmonary Hypertension
  • 1 Pulmonary Hypertension
  • 2 Warburg Effect and Pulmonary Hypertension
  • 3 Glucose Metabolism, Pentose Shunt, and Glucose-ÂƯ6-ÂƯPhosphate Dehydrogenase in Pulmonary Hypertension
  • 3.1 Glucose Metabolism is Altered in Pulmonary Hypertension
  • 3.2 Glucose-6-Phosphate Dehydrogenase Inhibition Relaxes Pulmonary Arteries, Reduces Inflammatory Cytokines and Cell Proliferation, and Induces Cell Apoptosis3.3 Glucose-6-Phosphate Dehydrogenase Inhibitor Treatment Reduces Pulmonary Hypertension
  • 4 G6PD and CD133 (+) Cells in Pulmonary Hypertension
  • 4.1 CD133 (+) Cells
  • 4.2 Glucose Metabolism and G6PD in CD133 (+) Cells
  • 4.3 CD133 (+) Cells Increase in Pulmonary Hypertension
  • 4.4 CD133 (+) Cells Exacerbate Pulmonary Arterial Hypertension
  • References
  • Redox Regulation of the Superoxide Dismutases SOD3 and SOD2 in the Pulmonary Circulation1 Introduction
  • 2 The Extracellular SOD3 Enzyme
  • 2.1 Characterization of SOD3
  • 2.2 Redox Regulation of SOD3
  • 2.2.1 Intrasubunit Disulfide Bonds
  • 2.2.2 Intersubunit Disulfide Bond
  • 2.2.3 Proteolytic Cleavage of SOD3
  • 2.3 Regulation of SOD3 Activity
  • 2.4 Regulation of SOD3 Gene Expression
  • 2.5 Redox Regulation by SOD3 in Pulmonary Hypertension
  • 3 The Mitochondrial SOD2 Enzyme
  • 3.1 Characterization of SOD2

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