Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study

<b>Background</b>: The current pharmacological treatments for Immunoglobulin A nephropathy (IgAN) demonstrate limited effectiveness and may cause serious side effects. This study aimed to explore novel potential drug targets for IgAN. <b>Methods</b>: We utilized summarized da...

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Main Authors: Limei Xiong, Hui Zhang, Yannan Guo, Yuhong Tao
Format: Article
Language:English
Published: MDPI AG 2025-02-01
Series:Biomedicines
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Online Access:https://www.mdpi.com/2227-9059/13/3/581
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author Limei Xiong
Hui Zhang
Yannan Guo
Yuhong Tao
author_facet Limei Xiong
Hui Zhang
Yannan Guo
Yuhong Tao
author_sort Limei Xiong
collection DOAJ
description <b>Background</b>: The current pharmacological treatments for Immunoglobulin A nephropathy (IgAN) demonstrate limited effectiveness and may cause serious side effects. This study aimed to explore novel potential drug targets for IgAN. <b>Methods</b>: We utilized summarized data from a recent genome-wide association study on IgAN, cis-expression quantitative trait loci data for druggable genes obtained from the eQTLGen Consortium, and DNA methylation quantitative trait loci data derived from the GoDMC database. Two-sample Mendelian randomization (MR) analysis, Bayesian colocalization, and mediation analysis through a two-step MR approach were performed to investigate their causal relationships. <b>Results</b>: Two-sample MR and colocalization analyses demonstrated that the expression of <i>HLA-DPA1</i> and <i>C4A</i> was associated with an increased risk of IgAN. In contrast, <i>TUBB</i>, <i>CYP21A2</i>, and <i>C4B</i> were associated with a decreased risk of IgAN. Mediation analysis revealed that the expression of <i>HLA-DPA1</i> acted as a mediator in the potential causal relationship between three DNA methylation sites (cg01140143, cg08898074, and cg12168509) and IgAN, with mediated proportions of 33.74% (95% CI 1.64–73.27), 41.67% (95% CI 20.78–66.97), and 50.34% (95% CI 27.89–74.76), respectively. <b>Conclusions</b>: Several druggable genes and DNA methylation sites were identified to show potential causal associations with IgAN risk and may be targeted for drug development. Nevertheless, additional experimental validation is warranted to clarify the specific roles of DNA methylation and the identified druggable genes in the pathogenesis of IgAN.
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spelling doaj-art-c5cb960b07944669aa4685cac986bb8b2025-08-20T03:43:33ZengMDPI AGBiomedicines2227-90592025-02-0113358110.3390/biomedicines13030581Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization StudyLimei Xiong0Hui Zhang1Yannan Guo2Yuhong Tao3Division of Nephrology, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, ChinaDivision of Nephrology, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, ChinaDivision of Nephrology, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, ChinaDivision of Nephrology, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China<b>Background</b>: The current pharmacological treatments for Immunoglobulin A nephropathy (IgAN) demonstrate limited effectiveness and may cause serious side effects. This study aimed to explore novel potential drug targets for IgAN. <b>Methods</b>: We utilized summarized data from a recent genome-wide association study on IgAN, cis-expression quantitative trait loci data for druggable genes obtained from the eQTLGen Consortium, and DNA methylation quantitative trait loci data derived from the GoDMC database. Two-sample Mendelian randomization (MR) analysis, Bayesian colocalization, and mediation analysis through a two-step MR approach were performed to investigate their causal relationships. <b>Results</b>: Two-sample MR and colocalization analyses demonstrated that the expression of <i>HLA-DPA1</i> and <i>C4A</i> was associated with an increased risk of IgAN. In contrast, <i>TUBB</i>, <i>CYP21A2</i>, and <i>C4B</i> were associated with a decreased risk of IgAN. Mediation analysis revealed that the expression of <i>HLA-DPA1</i> acted as a mediator in the potential causal relationship between three DNA methylation sites (cg01140143, cg08898074, and cg12168509) and IgAN, with mediated proportions of 33.74% (95% CI 1.64–73.27), 41.67% (95% CI 20.78–66.97), and 50.34% (95% CI 27.89–74.76), respectively. <b>Conclusions</b>: Several druggable genes and DNA methylation sites were identified to show potential causal associations with IgAN risk and may be targeted for drug development. Nevertheless, additional experimental validation is warranted to clarify the specific roles of DNA methylation and the identified druggable genes in the pathogenesis of IgAN.https://www.mdpi.com/2227-9059/13/3/581druggable genesDNA methylationimmunoglobulin A nephropathyMendelian randomization analysisgenetic susceptibility
spellingShingle Limei Xiong
Hui Zhang
Yannan Guo
Yuhong Tao
Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study
Biomedicines
druggable genes
DNA methylation
immunoglobulin A nephropathy
Mendelian randomization analysis
genetic susceptibility
title Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study
title_full Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study
title_fullStr Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study
title_full_unstemmed Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study
title_short Identification of Potential Drug Targets for Immunoglobulin A Nephropathy: A Mendelian Randomization Study
title_sort identification of potential drug targets for immunoglobulin a nephropathy a mendelian randomization study
topic druggable genes
DNA methylation
immunoglobulin A nephropathy
Mendelian randomization analysis
genetic susceptibility
url https://www.mdpi.com/2227-9059/13/3/581
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