Evidence map›Paper›PMID 38890564›Full record

ArticleBMC genomics2024

Susceptibility gene identification and risk evaluation model construction by transcriptome-wide association analysis for salt sensitivity of blood pressure.

Han Qi, Yun-Yi Xie, Xiao-Jun Yang, Juan Xia, Kuo Liu, Feng-Xu Zhang, Wen-Juan Peng, Fu-Yuan Wen, Bing-Xiao Li, Bo-Wen Zhang and 6 more

Abstract read
In one paragraph

Article in BMC genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Han QiDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Yun-Yi XieDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Xiao-Jun YangDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Juan XiaDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Kuo LiuDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Feng-Xu ZhangDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Wen-Juan PengDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Fu-Yuan WenDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Bing-Xiao LiDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Bo-Wen ZhangDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Xin-Yue YaoDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Bo-Ya LiDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China.
Hong-Dao MengFaculty of Information Technology, Beijing University of Technology, Beijing, 100124, China.
Zu-Min ShiHuman Nutrition Department, College of Health Sciences, QU Health, Qatar University, Doha, Qatar.
Yang WangDepartment of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
Ling ZhangDepartment of Epidemiology and Health Statistics, School of Public Health, Beijing Municipal Key Laboratory of Clinical Epidemiology, Capital Medical University, No.10 Youanmenwai, Beijing, 100069, China. zlilyepi@ccmu.edu.cn.

Funding

National Natural Science Foundation of China 82273708
6 · The paper itself

Abstract

backgroundSalt sensitivity of blood pressure (SSBP) is an intermediate phenotype of hypertension and is a predictor of long-term cardiovascular events and death. However, the genetic structures of SSBP are uncertain, and it is difficult to precisely diagnose SSBP in population. So, we aimed to identify genes related to susceptibility to the SSBP, construct a risk evaluation model, and explore the potential functions of these genes. METHODS AND

resultsA genome-wide association study of the systemic epidemiology of salt sensitivity (EpiSS) cohort was performed to obtain summary statistics for SSBP. Then, we conducted a transcriptome-wide association study (TWAS) of 12 tissues using FUSION software to predict the genes associated with SSBP and verified the genes with an mRNA microarray. The potential roles of the genes were explored. Risk evaluation models of SSBP were constructed based on the serial P value thresholds of polygenetic risk scores (PRSs), polygenic transcriptome risk scores (PTRSs) and their combinations of the identified genes and genetic variants from the TWAS. The TWAS revealed that 2605 genes were significantly associated with SSBP. Among these genes, 69 were differentially expressed according to the microarray analysis. The functional analysis showed that the genes identified in the TWAS were enriched in metabolic process pathways. The PRSs were correlated with PTRSs in the heart atrial appendage, adrenal gland, EBV-transformed lymphocytes, pituitary, artery coronary, artery tibial and whole blood. Multiple logistic regression models revealed that a PRS of P < 0.05 had the best predictive ability compared with other PRSs and PTRSs. The combinations of PRSs and PTRSs did not significantly increase the prediction accuracy of SSBP in the training and validation datasets.

conclusionsSeveral known and novel susceptibility genes for SSBP were identified via multitissue TWAS analysis. The risk evaluation model constructed with the PRS of susceptibility genes showed better diagnostic performance than the transcript levels, which could be applied to screen for SSBP high-risk individuals.

Indexed as

Blood PressureGenetic Predisposition to DiseaseGenome-Wide Association StudyFemaleGene Expression ProfilingHumansHypertensionMalePolymorphism, Single NucleotideRisk AssessmentSodium Chloride, DietaryTranscriptomeSodium Chloride, DietaryEpiSS studyPolygenetic risk scoresPolygenic transcriptome risk scoresSalt sensitivity of blood pressureTranscriptome-wide association study

Identifiers

PMID38890564
PMCPMC11184770

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.