Genetic evidence for amlodipine’s protective role in gastroesophageal reflux disease: A focus on CACNB2
This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enric...
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| Published in | PloS one Vol. 20; no. 2; p. e0309805 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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United States
Public Library of Science
18.02.2025
Public Library of Science (PLoS) |
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| Abstract | This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network.
Publicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings.
The MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes.
This study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. |
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| AbstractList | This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network. Publicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings. The MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes. This study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. Objective This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network. Methods Publicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings. Results The MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes. Conclusion This study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. ObjectiveThis study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network.MethodsPublicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings.ResultsThe MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes.ConclusionThis study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network.OBJECTIVEThis study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network.Publicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings.METHODSPublicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings.The MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes.RESULTSThe MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes.This study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes.CONCLUSIONThis study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network. Publicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings. The MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812-0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes. This study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. Objective This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using a bidirectional Mendelian Randomization (MR) approach and to explore the underlying genetic and molecular mechanisms through functional enrichment analysis and the construction of a competing endogenous RNA (ceRNA) network. Methods Publicly available GWAS datasets from the Neale Lab consortium were used, including data on amlodipine (13,693 cases, 323,466 controls) and GERD (14,316 cases, 322,843 controls). Genome-wide significant SNPs were selected as instrumental variables and clustered by linkage disequilibrium. MR analysis was conducted using R software with all five methods. Sensitivity analyses assessed pleiotropy and heterogeneity. Drug target genes were analyzed using GO and KEGG pathways. GeneMANIA was used for network visualization, and a ceRNA network was constructed with Cytoscape. Differential gene expression analysis on GERD-related datasets from GEO validated the findings. Results The MR analysis indicated a significant negative association between genetically predicted amlodipine use and GERD risk (IVW OR = 0.872, 95% CI = 0.812–0.937, P = 0.0002). Sensitivity analyses confirmed the robustness of these findings, showing no evidence of pleiotropy or heterogeneity. The enrichment analysis identified key biological processes and pathways involving calcium ion transport and signaling. The ceRNA network highlighted core targets such as CACNB2, which were further validated by differential expression analysis intersecting drug target genes with GERD-related gene expression changes. Conclusion This study provides robust evidence of a protective effect of amlodipine against GERD, supported by genetic and molecular analyses. The findings suggest that calcium channel blockers like amlodipine could be repurposed for GERD treatment. The identification of CACNB2 and other core targets in the ceRNA network offers novel insights into the pathophysiology of GERD and potential therapeutic targets, paving the way for personalized medicine approaches to improve patient outcomes. |
| Audience | Academic |
| Author | Jiang, Shuyue Zhang, Liuzhao Chu, Quanwang Shao, Bo |
| AuthorAffiliation | District Head Quarter (DHQ) Hospital Charsadda / University of Peshawar, PAKISTAN 1 Department of Critical Care Medicine, Anhui Jing’an Medicine Hospital, Hefei, China 2 Department of Pathology, Anhui Provincial Children’s Hospital, Hefei, China |
| AuthorAffiliation_xml | – name: 1 Department of Critical Care Medicine, Anhui Jing’an Medicine Hospital, Hefei, China – name: 2 Department of Pathology, Anhui Provincial Children’s Hospital, Hefei, China – name: District Head Quarter (DHQ) Hospital Charsadda / University of Peshawar, PAKISTAN |
| Author_xml | – sequence: 1 givenname: Liuzhao surname: Zhang fullname: Zhang, Liuzhao – sequence: 2 givenname: Quanwang surname: Chu fullname: Chu, Quanwang – sequence: 3 givenname: Shuyue surname: Jiang fullname: Jiang, Shuyue – sequence: 4 givenname: Bo orcidid: 0000-0002-3757-4214 surname: Shao fullname: Shao, Bo |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39965006$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright: © 2025 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. COPYRIGHT 2025 Public Library of Science 2025 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2025 Zhang et al 2025 Zhang et al 2025 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1371/journal.pone.0309805 |
| PMID | 39965006 |
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| PublicationDate | 2025-02-18 |
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| Snippet | This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease (GERD) using... Objective This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease... ObjectiveThis study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease... Objective This study aims to elucidate the causal relationship between genetically predicted amlodipine use and the risk of gastroesophageal reflux disease... |
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| SubjectTerms | Amlodipine Amlodipine - pharmacology Amlodipine - therapeutic use Analysis Angina pectoris Antihypertensive drugs Biological activity Biology and Life Sciences Calcium Calcium channel blockers Calcium channels Calcium signalling Calcium transport Computer and Information Sciences Datasets Disease Diseases Dosage and administration Drug therapy Esophagus Gastroesophageal reflux Gastroesophageal Reflux - drug therapy Gastroesophageal Reflux - genetics Gastroesophageal Reflux - prevention & control Gastrointestinal agents Gene expression Gene Regulatory Networks Gene set enrichment analysis Genes Genetic analysis Genetic aspects Genetics Genome-Wide Association Study Genomes Genomic analysis Heterogeneity Humans Ion transport Linkage analysis Linkage disequilibrium Medicine and Health Sciences Mendelian Randomization Analysis MicroRNAs Molecular modelling Ontology Pathophysiology Patient outcomes Pharmacogenetics Physical Sciences Pleiotropy Polymorphism, Single Nucleotide Precision medicine RNA Sensitivity analysis Single-nucleotide polymorphism Software Therapeutic targets |
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| Title | Genetic evidence for amlodipine’s protective role in gastroesophageal reflux disease: A focus on CACNB2 |
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