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Pulmonary arterial hypertension is a severe and progressive disorder affecting the blood vessels in the lungs. Typically, symptoms first appear at around 30–40 years of age and, without treatment, can lead to fatal heart disease within a few years. Genetic studies over the past decade have identified numerous genes that contribute to disease progression but, for many sufferers, the underlying genetic cause remains elusive. The collection of reviews and original research articles contained within this book provide an overview of recent advancements in understanding the genetic risk factors for pulmonary arterial hypertension. We further examine the emerging interplay between genetic variants and clinical outcomes, providing a framework for new treatments and improved patient care.

Research & information: general --- Biology, life sciences --- Genetics (non-medical) --- pulmonary arterial hypertension --- massive parallel sequencing --- NGS --- digenic inheritance --- and genetics --- BMPR2 promoter --- pathogenic variant --- heritable pulmonary arterial hypertension --- genetic analysis --- NGS gene panel --- BMPR2 --- TBX4 --- GDF2 --- EIF2AK4 --- genomics --- pediatrics --- lung disease --- endothelial cells --- smooth muscle cells --- DNA damage --- DNA repair --- expression quantitative trait locus --- eQTL --- blood --- genetics --- exome sequencing --- molecular genetics --- paediatrics --- bone morphogenetic protein receptor type 2 --- heritable --- familial --- estrogen --- estradiol --- penetrance --- gender --- PAH --- forward phenotyping --- forward genetics --- reverse genetics --- reverse phenotyping --- intermediate phenotypes --- whole-genome sequencing --- epigenetic inheritance --- genetic heterogeneity --- phenotypic heterogeneity --- pulmonary hypertension --- bone morphogenetic protein receptor 2 --- signaling --- repurposed drugs --- pharmaceuticals --- miRNA --- clinical trials --- n/a

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Pulmonary arterial hypertension is a severe and progressive disorder affecting the blood vessels in the lungs. Typically, symptoms first appear at around 30–40 years of age and, without treatment, can lead to fatal heart disease within a few years. Genetic studies over the past decade have identified numerous genes that contribute to disease progression but, for many sufferers, the underlying genetic cause remains elusive. The collection of reviews and original research articles contained within this book provide an overview of recent advancements in understanding the genetic risk factors for pulmonary arterial hypertension. We further examine the emerging interplay between genetic variants and clinical outcomes, providing a framework for new treatments and improved patient care.

Research & information: general --- Biology, life sciences --- Genetics (non-medical) --- pulmonary arterial hypertension --- massive parallel sequencing --- NGS --- digenic inheritance --- and genetics --- BMPR2 promoter --- pathogenic variant --- heritable pulmonary arterial hypertension --- genetic analysis --- NGS gene panel --- BMPR2 --- TBX4 --- GDF2 --- EIF2AK4 --- genomics --- pediatrics --- lung disease --- endothelial cells --- smooth muscle cells --- DNA damage --- DNA repair --- expression quantitative trait locus --- eQTL --- blood --- genetics --- exome sequencing --- molecular genetics --- paediatrics --- bone morphogenetic protein receptor type 2 --- heritable --- familial --- estrogen --- estradiol --- penetrance --- gender --- PAH --- forward phenotyping --- forward genetics --- reverse genetics --- reverse phenotyping --- intermediate phenotypes --- whole-genome sequencing --- epigenetic inheritance --- genetic heterogeneity --- phenotypic heterogeneity --- pulmonary hypertension --- bone morphogenetic protein receptor 2 --- signaling --- repurposed drugs --- pharmaceuticals --- miRNA --- clinical trials --- pulmonary arterial hypertension --- massive parallel sequencing --- NGS --- digenic inheritance --- and genetics --- BMPR2 promoter --- pathogenic variant --- heritable pulmonary arterial hypertension --- genetic analysis --- NGS gene panel --- BMPR2 --- TBX4 --- GDF2 --- EIF2AK4 --- genomics --- pediatrics --- lung disease --- endothelial cells --- smooth muscle cells --- DNA damage --- DNA repair --- expression quantitative trait locus --- eQTL --- blood --- genetics --- exome sequencing --- molecular genetics --- paediatrics --- bone morphogenetic protein receptor type 2 --- heritable --- familial --- estrogen --- estradiol --- penetrance --- gender --- PAH --- forward phenotyping --- forward genetics --- reverse genetics --- reverse phenotyping --- intermediate phenotypes --- whole-genome sequencing --- epigenetic inheritance --- genetic heterogeneity --- phenotypic heterogeneity --- pulmonary hypertension --- bone morphogenetic protein receptor 2 --- signaling --- repurposed drugs --- pharmaceuticals --- miRNA --- clinical trials

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Heart failure prevalence continues to rise globally. Regardless of the underlying etiology, heart failure remains a progressive disease, largely irreversible and end-stage heart failure requires transplantation. Book focuses on the challenges and recent advances of diagnosis, treatment and prevention of heart failure with or without associated comorbidities. We hope that readers will appreciate the wide breadth of topics and clinical utility of the articles and reviews included to this book collection.

biomarkers --- ST-segment elevation myocardial infarction --- preserved left ventricular ejection fraction --- reduced left ventricular ejection fraction --- heart failure --- NT-proBNP --- soluble ST2 --- galectin-3 --- matrix metalloproteinases --- tissue inhibitors of metalloproteinases --- mortality --- ejection fraction --- cardiopulmonary exercise test --- ventilatory inefficiency --- angiotensin receptor–neprilysin inhibitor --- echocardiography --- HFrEF --- risk stratification --- left ventricle end-diastolic diameter --- E/e’ ratio --- left ventricle outflow tract velocity-time integral --- hospitalization predictor --- short-term prognosis --- heart failure readmission --- acute myocardial infarction --- blood biomarkers --- diagnosis --- congestion --- clinical assessment --- preserved ejection fraction --- type 2 diabetes mellitus --- myocardial infarction --- chronic heart failure --- heart rate variability --- 2D echocardiography --- 24-h ECG monitoring --- chronic kidney disease --- pulmonary hypertension --- arteriovenous fistulas --- overhydration --- heart transplant --- cardiac allograft vasculopathy --- heart transplant rejection --- transthoracic echocardiography --- longitudinal strain --- sensing parameters --- pacing parameters --- adverse left ventricular remodeling --- left ventricular-arterial coupling --- fatty liver --- cardiovascular disease --- fibrosis --- epicardial fat --- left atrial strain --- edema --- dilated cardiomyopathy --- fluid management --- endothelial dysfunction --- n/a --- angiotensin receptor-neprilysin inhibitor --- E/e' ratio

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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.

Technology: general issues --- Biotechnology --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(-) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(-) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages

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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.

endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(–) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- n/a --- LDL(-)