Despite the blaze of advancing knowledge on its complex genetic architecture, hypertension remains an elusive condition. Genetic studies of blood pressure have yielded bitter-sweet results thus far with the identification of more than 2,000 genetic loci, though the candidate causal genes and biological pathways remain largely unknown. The era of big data and sophisticated statistical tools has propelled insights into pathophysiology and causal inferences. However, new genetic risk tools for hypertension are the tip of the iceberg, and applications of genomic technology are likely to proliferate. We review the genomics of hypertension, exploring the significant milestones in our current understanding of this condition and the progress towards personalised treatment and management for hypertension.
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http://dx.doi.org/10.1017/pcm.2025.1 | DOI Listing |
Genetic factors contribute to the development of metabolic syndrome and subsequent arterial hypertension (AH). The study of the T786C polymorphism of the endothelial nitric oxide synthase (eNOS) gene in arterial hypertension is important as its correlation with adipokine imbalance is a novelty area to find associations between hypertension development, obesity, and heredity. The purpose of the current study was to investigate serum adipokines levels, depending on the T786C polymorphism of the eNOS in patients with arterial hypertension.
View Article and Find Full Text PDFCamb Prism Precis Med
February 2025
William Harvey Research Institute, Queen Mary University of London, London, UK.
Despite the blaze of advancing knowledge on its complex genetic architecture, hypertension remains an elusive condition. Genetic studies of blood pressure have yielded bitter-sweet results thus far with the identification of more than 2,000 genetic loci, though the candidate causal genes and biological pathways remain largely unknown. The era of big data and sophisticated statistical tools has propelled insights into pathophysiology and causal inferences.
View Article and Find Full Text PDFSci Rep
March 2025
Estonian Genome Centre, Institute of Genomics, University of Tartu, Riia 23b, 51010, Tartu, Estonia.
The purpose of this study was to find metabolic changes associated with incident hypertension in the volunteer-based Estonian Biobank. We used a subcohort of the Estonian Biobank where metabolite levels had been measured by mass-spectrometry (LC-MS, Metabolon platform). We divided annotated metabolites of 989 individuals into KEGG pathways, followed by principal component analysis of metabolites in each pathway, resulting in a dataset of 91 pathway components.
View Article and Find Full Text PDFMedicine (Baltimore)
March 2025
Phase I Clinical Trial Center, Xiangya Hospital, Central South University, Changsha, China.
The causal association between pulmonary arterial hypertension (PAH) and autoimmune diseases remains uncertain. This study aimed to assess the causal associations between PAH and autoimmune diseases using bidirectional Mendelian randomization (MR) analyses. Genome-wide association summary statistics for PAH, asthma, myasthenia gravis, rheumatoid arthritis (RA), systemic lupus erythematosus, and type 1 diabetes mellitus were obtained from publicly accessible databases.
View Article and Find Full Text PDFCirc Rep
March 2025
Department of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute Osaka Japan.
Background: Because Regnase-1, encoded by , suppresses the development of pulmonary arterial hypertension (PAH) by controlling pro-inflammatory cytokines, we aimed to identify variants in patients with PAH.
Methods And Results: We analyzed whole-genome sequence data of patients with PAH to search for disease-associated variants. The Regnase-1 p.
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