ReviewNature reviews. Nephrology2026
The genetics of hypertension.
Review in Nature reviews. Nephrology, 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 3 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association BetweenInternational journal of environmental research and public health · 2026Pooled it
- Review
- Long-acting RNAi therapeutics in hypertension: limitations of single-target AGT silencing and rational multi-target synergistic strategies.Frontiers in pharmacology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertension, or persistently elevated blood pressure, affects about one third of the adult population worldwide and causes approximately 8.5 million deaths annually. Family studies have demonstrated that blood pressure shows substantial heritability, suggesting that genetic factors contribute to hypertension. Linkage studies and next-generation sequencing efforts have identified several variants with large effect sizes that cause rare monogenic hypertension syndromes. These syndromes often present with early onset and typically affect adrenal and renal regulation of salt reabsorption. In addition, somatic (tumour-specific) mutations have been identified in hormone-producing tumours that cause hypertension (phaeochromocytomas, aldosterone-producing adenomas, cortisol-producing adenomas, pituitary adenomas, reninomas). However, most cases of hypertension are polygenic. Large genome-wide association studies have identified many variants with small effect sizes that add to our understanding of blood pressure as a complex trait. Epigenetic mechanisms also influence gene expression and contribute to blood-pressure alterations. Several proteins that are affected by Mendelian diseases are targets of existing antihypertensive drugs and other such proteins may be good candidates for future drug development.
Indexed as
Identifiers
41219524What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.