By Marc Humbert, Oleg V. Evgenov, Johannes-Peter Stasch
This quantity specializes in present evidence-based pharmacological remedies of varied varieties of pulmonary high blood pressure and gives a entire evaluation of the newest advancements during this quarter. the 1st a part of the booklet covers the definition, type, pathophysiology, pathology, biomarkers and animal versions of the illness, therefore laying the conceptual foundation for what follows. the center part offers an outline of the confirmed treatments, corresponding to calcium channel blockers, prostanoids, endothelin receptor antagonists, phosphodiesterase-5 inhibitors and inhaled nitric oxide. The final part explores novel pathways and rising healing methods together with soluble guanylate cyclase stimulators, Rho-kinase inhibitors, inhibitors of serotonin receptors and transporters, peptide progress elements, vasoactive peptides, modulators of redox equilibrium and cyclic nucleotide homeostasis, in addition to immunosuppressive and anti-proliferative brokers. specific awareness is given to the medical purposes of those experimental treatments, which are at the horizon. The e-book therefore spans the continuum from easy technology to scientific applications.
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Abbreviations BH4 BMP-RII cAMP cGMP COX EGFR eNOS ET-1 ETA ETB FeNO GTP HAPE HHT HIF HIV IL ISCU1/2 KL LO LV MAPK miR NO• NOX Tetrahydrobiopterin Bone morphogenetic protein receptor II Cyclic adenosine monophosphate Cyclic guanosine monophosphate Cyclooxygenase Epidermal growth factor receptor Endothelial nitric oxide synthase Endothelin-1 Endothelin-type A receptor Endothelin-type B receptor Iron-nitrosyl Guanosine triphosphate High altitude pulmonary edema syndrome Hereditary hemorrhagic telangiectasia Hypoxia-inducible factor Human immunodeficiency virus Interleukin Iron–sulfur cluster assembly proteins Kruppel-like factor Lipooxygenases Left ventricle Mitogen-activated protein kinase MicroRNA Nitric oxide NADPH oxidase 33 34 37 37 40 42 43 44 46 48 50 52 52 Pulmonary Hypertension: Pathophysiology and Signaling Pathways O2À O2NOOÀ ONOOÀ PAEC PAH PDE PDGF PDK PG PH PKG PPAR-γ PSMC PTPC ROS RV sGC SOD TAPSE TGF TXA2 VEGF • 33 Superoxide Peroxynitrate Peroxynitrite Pulmonary artery endothelial cells Pulmonary arterial hypertension Phosphodiesterase inhibitor Platelet-derived growth factor Pyruvate dehydrogenase kinase Prostaglandin Pulmonary hypertension Protein kinase G Peroxisome proliferator-activated receptor Pulmonary artery smooth muscle cells Permeability transition pore complex Reactive oxygen species Right ventricle Soluble guanylyl cyclase Superoxide dismutase Tricuspid annular plane systolic excursion Transforming growth factor Thromboxane Vascular endothelial growth factor 1 Introduction Maladaptive changes to the phenotype of pulmonary arterioles resulting in pulmonary vascular dysfunction, right ventricular (RV) pressure loading, and, ultimately, right heart failure are a central pathophysiological mechanism leading to the development of clinically evident pulmonary hypertension (PH).
Abbreviations BH4 BMP-RII cAMP cGMP COX EGFR eNOS ET-1 ETA ETB FeNO GTP HAPE HHT HIF HIV IL ISCU1/2 KL LO LV MAPK miR NO• NOX Tetrahydrobiopterin Bone morphogenetic protein receptor II Cyclic adenosine monophosphate Cyclic guanosine monophosphate Cyclooxygenase Epidermal growth factor receptor Endothelial nitric oxide synthase Endothelin-1 Endothelin-type A receptor Endothelin-type B receptor Iron-nitrosyl Guanosine triphosphate High altitude pulmonary edema syndrome Hereditary hemorrhagic telangiectasia Hypoxia-inducible factor Human immunodeficiency virus Interleukin Iron–sulfur cluster assembly proteins Kruppel-like factor Lipooxygenases Left ventricle Mitogen-activated protein kinase MicroRNA Nitric oxide NADPH oxidase 33 34 37 37 40 42 43 44 46 48 50 52 52 Pulmonary Hypertension: Pathophysiology and Signaling Pathways O2À O2NOOÀ ONOOÀ PAEC PAH PDE PDGF PDK PG PH PKG PPAR-γ PSMC PTPC ROS RV sGC SOD TAPSE TGF TXA2 VEGF • 33 Superoxide Peroxynitrate Peroxynitrite Pulmonary artery endothelial cells Pulmonary arterial hypertension Phosphodiesterase inhibitor Platelet-derived growth factor Pyruvate dehydrogenase kinase Prostaglandin Pulmonary hypertension Protein kinase G Peroxisome proliferator-activated receptor Pulmonary artery smooth muscle cells Permeability transition pore complex Reactive oxygen species Right ventricle Soluble guanylyl cyclase Superoxide dismutase Tricuspid annular plane systolic excursion Transforming growth factor Thromboxane Vascular endothelial growth factor 1 Introduction Maladaptive changes to the phenotype of pulmonary arterioles resulting in pulmonary vascular dysfunction, right ventricular (RV) pressure loading, and, ultimately, right heart failure are a central pathophysiological mechanism leading to the development of clinically evident pulmonary hypertension (PH).
6 Mitochondrial Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Peroxisome Proliferator-Activated Receptor-γ . . . . . . . . . . . . . . . . . . . . 8 MicroRNA-Mediated Regulation of Cellular Responses to Hypoxia . . . . . . . . 4 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . .