ArticleNature communications2024
Genetic imputation of kidney transcriptome, proteome and multi-omics illuminates new blood pressure and hypertension targets.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Urate-lowering effects of losartan: a meta-analysis of randomised controlled trials and target trial emulation.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Pooled it
- Quantifying direct genetic signal captured by principal component adjustment.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Shorter kidney telomeres are associated with nephrosclerosis by an epigenetic signature.Cardiovascular research · 2026Article
- The genetics of hypertension.Nature reviews. Nephrology · 2026Review
- Article
- From albuminuria to multi-omics signatures: emerging biomarkers and drug targets for early-stage chronic kidney disease.Frontiers in pharmacology · 2026Review
- A network-guided penalized regression with application to proteomics data.Bioinformatics advances · 2026Article
- The proteogenomic landscape of the human kidney and implications for cardio-kidney-metabolic health.Nature medicine · 2025 · on this mapArticle
- The carbonic anhydrase 3 protein in urine: a potential biomarker to monitor atherosclerotic renal artery stenosis.BMC nephrology · 2025Article
- Metabolomic Understanding of variable risk factors for kidney cancer: a two-sample Mendelian randomization study.Discover oncology · 2025Article
- Renal-Cardiac Crosstalk in the Pathogenesis and Progression of Heart Failure.Circulation research · 2025Review
- Kidney multiome-based genetic scorecard reveals convergent coding and regulatory variants.Science (New York, N.Y.) · 2025Article
- scTWAS Atlas: an integrative knowledgebase of single-cell transcriptome-wide association studies.Nucleic acids research · 2025Article
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
39 authors at 11 institutions in 6 countries.
Funding
Abstract
Genetic mechanisms of blood pressure (BP) regulation remain poorly defined. Using kidney-specific epigenomic annotations and 3D genome information we generated and validated gene expression prediction models for the purpose of transcriptome-wide association studies in 700 human kidneys. We identified 889 kidney genes associated with BP of which 399 were prioritised as contributors to BP regulation. Imputation of kidney proteome and microRNAome uncovered 97 renal proteins and 11 miRNAs associated with BP. Integration with plasma proteomics and metabolomics illuminated circulating levels of myo-inositol, 4-guanidinobutanoate and angiotensinogen as downstream effectors of several kidney BP genes (SLC5A11, AGMAT, AGT, respectively). We showed that genetically determined reduction in renal expression may mimic the effects of rare loss-of-function variants on kidney mRNA/protein and lead to an increase in BP (e.g., ENPEP). We demonstrated a strong correlation (r = 0.81) in expression of protein-coding genes between cells harvested from urine and the kidney highlighting a diagnostic potential of urinary cell transcriptomics. We uncovered adenylyl cyclase activators as a repurposing opportunity for hypertension and illustrated examples of BP-elevating effects of anticancer drugs (e.g. tubulin polymerisation inhibitors). Collectively, our studies provide new biological insights into genetic regulation of BP with potential to drive clinical translation in hypertension.
Indexed as
Identifiers
What 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.