ArticleHypertension (Dallas, Tex. : 1979)2026
GWAS and Replication Analysis of Apparent Treatment-Resistant Hypertension.
Article in Hypertension (Dallas, Tex. : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Resistant Hypertension Variants Link to Hyperaldosteronism and Potassium Levels.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings.Molecules (Basel, Switzerland) · 2026Article
- Cardiovascular Genetic Epidemiology in the Genome-Wide Era: From Association Discovery to Mechanistic Dissection and Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Review
- Genetic factors contributing to atherosclerosis.Current opinion in cardiology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
backgroundResistant hypertension (RH), in which blood pressure remains elevated on ≥3 medications or controlled on ≥4 medications, increases the risk of adverse cardiovascular events nearly 50% more than primary hypertension. We sought to identify genetic drivers of RH in a reliable and generalizable manner.
methodsWe utilized FinnGen (discovery) and UKBB (UK Biobank, replication) data sets to identify potential genetic drivers of RH. Using standard RH definitions, we developed cohorts in each data set and performed genome-wide (genome-wide association studies) and transcriptome-wide association studies, as well as Mendelian randomization analysis to evaluate potential causal associations.
resultsWe replicated 5 genetic loci in
conclusionsWe identified distinct genetic variants associated with RH, including those implicating the role of hyperaldosteronism, highlighting distinct pathways and targets for more effectively treating RH.
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What OpenQuestion holds
Registered trials
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