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Arterial hypertension affects about 1 billion people worldwide and it is the strongest modifiable risk factor for cardiovascular disease and related disability. Since the initial discovery of rare monogenic disorders with large effects, the role of genomics has evolved into large genome-wide association studies detecting common variants with a modest effect size. Similarly, pharmacogenomics has emerged as a new tool for understanding variability in drug response, to maximize efficacy and reduce toxicity. This book presents the most recent advances in the field of genetics and genomics of arterial hypertension and their potential impact on clinical management. The book is a useful tool for clinicians but also to the research community and those who want to be updated in the field.
atrial natriuretic peptide --- T2238C variant --- endothelial dysfunction --- smooth muscle cells contraction --- platelet aggregation --- epigenetics --- cardiovascular diseases --- renin --- low-renin --- hypertension --- mineralocorticoid receptor --- genetics --- aldosterone --- essential hypertension --- blood pressure --- genome-wide association studies --- exome microarray --- next-generation sequencing --- rare variants --- rare-variants association testing --- burden test --- sequence kernel association test --- hypokalemia --- low renin hypertension --- monogenic hypertension --- Liddle syndrome --- SCNN1A --- SCNN1B --- SCNN1G --- non-coding RNA --- micro RNA --- primary aldosteronism --- aldosterone-producing adenoma --- transcriptome profiing --- DNA methylation --- histone modifications --- vascular smooth muscle cells --- endothelial cells --- Kruppel-like factor 15 --- left ventricular hypertrophy --- cardiac hypertrophy --- heart failure --- genetics of left ventricular hypertrophy --- fibromuscular dysplasia --- non atherosclerotic vascular stenosis --- PHACTR1 --- genetic association --- cervical artery dissection --- spontaneous coronary arteries dissection --- CRY1 --- CRY2 --- HSD3B1 --- HSD3B2 --- cardio-tonic steroids --- endogenous ouabain --- adducin --- renal damage --- African American --- ARMC5 --- GRK4 --- CACNA1D --- endocrine hypertension
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