ArticleJournal of clinical hypertension (Greenwich, Conn.)2025
Joint Analysis of Multiple Omics to Describe the Biological Characteristics of Resistant Hypertension.
Article in Journal of clinical hypertension (Greenwich, Conn.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Resistant hypertension (RH) may cause severe target organ damage and poses significant challenges in the field of hypertension prevention and treatment. Mining biological characteristics is crucial for exploring the pathogenesis of RH and for early diagnosis and treatment. Although several single-omics studies have been conducted on RH, its complex pathogenesis has only been partially elucidated. In this study, metabolomics, proteomics, and transcriptomics were jointly analyzed in healthy subjects and patients with hypertension and RH. The multi-omics analysis found that differential substances of RH were enriched in the HIF-1 signaling pathway and that differential substances such as ascorbic acid, reduced glutathione (GSH), choline, citric acid, transferrin receptor (TfR), Egl-9 family hypoxia-inducible factor 2 (EGLN2), and glutathione peroxidase 1 (GPX1) were screened out. The results of intergroup comparisons were as follows: RH versus N: ascorbic acid (Fold Change (FC):0.42, p < 0.01), GSH (FC:0.65, p < 0.05), choline (FC:1.32, p < 0.05), citric acid (FC:0.48, p < 0.001), TfR (FC2.32, p < 0.001), GPX1 (FC:16.02, p < 0.001), EGLN2 (FC:0.76, p < 0.001); RH versus EH: ascorbic acid (FC:0.52, p < 0.05), GSH (FC:0.55, p < 0.05), choline (FC:1.28, p < 0.05), citric acid (FC:0.59, p < 0.001), TfR (FC:1.71, p < 0.001), GPX1 (FC:2.11, p < 0.05), EGLN2 (FC:0.76, p < 0.05). These differential substances may reflect the biology of RH. This study provides multi-omics analysis for a deeper understanding of the complex molecular characteristics of RH, providing new insights into the pathogenesis, early diagnosis, and precise treatment of the disease.
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.