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Elucidating the genetic relationship between ulcerative colitis and diabetic kidney disease: a bidirectional Mendelian randomization study
Ulcerative colitis (UC) and diabetic kidney disease (DKD) are chronic disorders with multifaceted pathogenesis, posing significant challenges in clinical management. While substantial efforts have been made to investigate the individual causes of these diseases, the interplay between UC and DKD is n...
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Published in: | Frontiers in endocrinology (Lausanne) 2024-08, Vol.15, p.1435812 |
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description | Ulcerative colitis (UC) and diabetic kidney disease (DKD) are chronic disorders with multifaceted pathogenesis, posing significant challenges in clinical management. While substantial efforts have been made to investigate the individual causes of these diseases, the interplay between UC and DKD is not well understood. This study aims to elucidate the genetic association between UC and DKD through Mendelian randomization (MR) analysis, offering new insights into common biological pathways and potential clinical implications.
We conducted a bidirectional two-sample MR study utilizing data from large-scale genome-wide association studies (GWAS) for both UC and DKD. Instrumental variables (IVs) were meticulously selected according to genome-wide significance and stringent statistical criteria, ensuring robust causal inference. Various MR methodologies, including inverse variance weighting (IVW), were employed to assess the causal relationships between UC and DKD. Sensitivity analyses were also performed to validate the robustness of our findings.
Our analysis revealed a significant causal relationship between genetic predisposition to UC and increased susceptibility to DKD. Specifically, individuals with a genetic susceptibility to UC exhibited a 17.3% higher risk of developing DKD. However, we found no evidence of a causal link between DKD and the risk of developing UC. Additionally, we identified shared genetic risk factors and molecular pathways linking UC and DKD, thereby highlighting potential therapeutic targets.
This study underscores the intricate genetic interplay between UC and DKD, suggesting that individuals with UC may be at an elevated risk for developing DKD. Understanding these shared genetic pathways could facilitate the development of early detection strategies and targeted interventions for individuals at risk of DKD. Ultimately, these insights could lead to improved clinical outcomes for patients suffering from both conditions. |
doi_str_mv | 10.3389/fendo.2024.1435812 |
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We conducted a bidirectional two-sample MR study utilizing data from large-scale genome-wide association studies (GWAS) for both UC and DKD. Instrumental variables (IVs) were meticulously selected according to genome-wide significance and stringent statistical criteria, ensuring robust causal inference. Various MR methodologies, including inverse variance weighting (IVW), were employed to assess the causal relationships between UC and DKD. Sensitivity analyses were also performed to validate the robustness of our findings.
Our analysis revealed a significant causal relationship between genetic predisposition to UC and increased susceptibility to DKD. Specifically, individuals with a genetic susceptibility to UC exhibited a 17.3% higher risk of developing DKD. However, we found no evidence of a causal link between DKD and the risk of developing UC. Additionally, we identified shared genetic risk factors and molecular pathways linking UC and DKD, thereby highlighting potential therapeutic targets.
This study underscores the intricate genetic interplay between UC and DKD, suggesting that individuals with UC may be at an elevated risk for developing DKD. Understanding these shared genetic pathways could facilitate the development of early detection strategies and targeted interventions for individuals at risk of DKD. Ultimately, these insights could lead to improved clinical outcomes for patients suffering from both conditions.</description><identifier>ISSN: 1664-2392</identifier><identifier>EISSN: 1664-2392</identifier><identifier>DOI: 10.3389/fendo.2024.1435812</identifier><identifier>PMID: 39211444</identifier><language>eng</language><publisher>Switzerland: Frontiers Media S.A</publisher><subject>Colitis, Ulcerative - complications ; Colitis, Ulcerative - genetics ; diabetic kidney disease ; Diabetic Nephropathies - genetics ; Endocrinology ; genetic causality ; Genetic Predisposition to Disease ; genome-wide association studies (GWAS) ; Genome-Wide Association Study ; Humans ; Mendelian randomization ; Mendelian Randomization Analysis ; Polymorphism, Single Nucleotide ; Risk Factors ; ulcerative colitis</subject><ispartof>Frontiers in endocrinology (Lausanne), 2024-08, Vol.15, p.1435812</ispartof><rights>Copyright © 2024 Guo, Yu, Li, Zhang, Xiong and Wu.</rights><rights>Copyright © 2024 Guo, Yu, Li, Zhang, Xiong and Wu 2024 Guo, Yu, Li, Zhang, Xiong and Wu</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358062/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358062/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39211444$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Yaping</creatorcontrib><creatorcontrib>Yu, Hangxing</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhang, Taijun</creatorcontrib><creatorcontrib>Xiong, Weijian</creatorcontrib><creatorcontrib>Wu, Xili</creatorcontrib><title>Elucidating the genetic relationship between ulcerative colitis and diabetic kidney disease: a bidirectional Mendelian randomization study</title><title>Frontiers in endocrinology (Lausanne)</title><addtitle>Front Endocrinol (Lausanne)</addtitle><description>Ulcerative colitis (UC) and diabetic kidney disease (DKD) are chronic disorders with multifaceted pathogenesis, posing significant challenges in clinical management. While substantial efforts have been made to investigate the individual causes of these diseases, the interplay between UC and DKD is not well understood. This study aims to elucidate the genetic association between UC and DKD through Mendelian randomization (MR) analysis, offering new insights into common biological pathways and potential clinical implications.
We conducted a bidirectional two-sample MR study utilizing data from large-scale genome-wide association studies (GWAS) for both UC and DKD. Instrumental variables (IVs) were meticulously selected according to genome-wide significance and stringent statistical criteria, ensuring robust causal inference. Various MR methodologies, including inverse variance weighting (IVW), were employed to assess the causal relationships between UC and DKD. Sensitivity analyses were also performed to validate the robustness of our findings.
Our analysis revealed a significant causal relationship between genetic predisposition to UC and increased susceptibility to DKD. Specifically, individuals with a genetic susceptibility to UC exhibited a 17.3% higher risk of developing DKD. However, we found no evidence of a causal link between DKD and the risk of developing UC. Additionally, we identified shared genetic risk factors and molecular pathways linking UC and DKD, thereby highlighting potential therapeutic targets.
This study underscores the intricate genetic interplay between UC and DKD, suggesting that individuals with UC may be at an elevated risk for developing DKD. Understanding these shared genetic pathways could facilitate the development of early detection strategies and targeted interventions for individuals at risk of DKD. Ultimately, these insights could lead to improved clinical outcomes for patients suffering from both conditions.</description><subject>Colitis, Ulcerative - complications</subject><subject>Colitis, Ulcerative - genetics</subject><subject>diabetic kidney disease</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Endocrinology</subject><subject>genetic causality</subject><subject>Genetic Predisposition to Disease</subject><subject>genome-wide association studies (GWAS)</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Mendelian randomization</subject><subject>Mendelian Randomization Analysis</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><subject>ulcerative colitis</subject><issn>1664-2392</issn><issn>1664-2392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkU1PXCEUhkljU431D3TRsHQzU77ulxtjjG1NbLpp14QL586gDEyBqxl_Qn91T0fbKBs4L5znBV5CPnC2lLIfPk0QXVoKJtSSK9n0XLwhR7xt1ULIQRy8WB-Sk1JuGQ7F-DD078ghqpwrpY7I76swW-9M9XFF6xroCiJUb2mGgGKKZe23dIT6ABDpHCxklO-B2hR89YWa6KjzZtw33XkXYYd1AVPgjBo6eucz2L8kE-g3vDQEbyLN2Jc2_nHvQUud3e49eTuZUODkeT4mPz9f_bj8urj5_uX68uJm4STr6qJxZpq6YRRWdaztm8aBUKKT7Sh451rRNHwAlAU3Dn8KFeFY34BqmZRdx-UxuX7iumRu9Tb7jck7nYzXeyHllTYZXxNAT7IboXW9skwpx6XhjUBrJrFSICWyzp9Y23ncgLMQazbhFfT1TvRrvUr3mnPMjLUCCafPhJx-zVCq3vhiIQQTIc1FS4aRobsY8OjHl2b_Xf6lKf8A5S6lyg</recordid><startdate>20240815</startdate><enddate>20240815</enddate><creator>Guo, Yaping</creator><creator>Yu, Hangxing</creator><creator>Li, Ying</creator><creator>Zhang, Taijun</creator><creator>Xiong, Weijian</creator><creator>Wu, Xili</creator><general>Frontiers Media S.A</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20240815</creationdate><title>Elucidating the genetic relationship between ulcerative colitis and diabetic kidney disease: a bidirectional Mendelian randomization study</title><author>Guo, Yaping ; Yu, Hangxing ; Li, Ying ; Zhang, Taijun ; Xiong, Weijian ; Wu, Xili</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-d307t-5daff79b2c4706855de242736b217d625519e85521ad338d622d085e460337713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Colitis, Ulcerative - complications</topic><topic>Colitis, Ulcerative - genetics</topic><topic>diabetic kidney disease</topic><topic>Diabetic Nephropathies - genetics</topic><topic>Endocrinology</topic><topic>genetic causality</topic><topic>Genetic Predisposition to Disease</topic><topic>genome-wide association studies (GWAS)</topic><topic>Genome-Wide Association Study</topic><topic>Humans</topic><topic>Mendelian randomization</topic><topic>Mendelian Randomization Analysis</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk Factors</topic><topic>ulcerative colitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Yaping</creatorcontrib><creatorcontrib>Yu, Hangxing</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhang, Taijun</creatorcontrib><creatorcontrib>Xiong, Weijian</creatorcontrib><creatorcontrib>Wu, Xili</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Frontiers in endocrinology (Lausanne)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Yaping</au><au>Yu, Hangxing</au><au>Li, Ying</au><au>Zhang, Taijun</au><au>Xiong, Weijian</au><au>Wu, Xili</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elucidating the genetic relationship between ulcerative colitis and diabetic kidney disease: a bidirectional Mendelian randomization study</atitle><jtitle>Frontiers in endocrinology (Lausanne)</jtitle><addtitle>Front Endocrinol (Lausanne)</addtitle><date>2024-08-15</date><risdate>2024</risdate><volume>15</volume><spage>1435812</spage><pages>1435812-</pages><issn>1664-2392</issn><eissn>1664-2392</eissn><abstract>Ulcerative colitis (UC) and diabetic kidney disease (DKD) are chronic disorders with multifaceted pathogenesis, posing significant challenges in clinical management. While substantial efforts have been made to investigate the individual causes of these diseases, the interplay between UC and DKD is not well understood. This study aims to elucidate the genetic association between UC and DKD through Mendelian randomization (MR) analysis, offering new insights into common biological pathways and potential clinical implications.
We conducted a bidirectional two-sample MR study utilizing data from large-scale genome-wide association studies (GWAS) for both UC and DKD. Instrumental variables (IVs) were meticulously selected according to genome-wide significance and stringent statistical criteria, ensuring robust causal inference. Various MR methodologies, including inverse variance weighting (IVW), were employed to assess the causal relationships between UC and DKD. Sensitivity analyses were also performed to validate the robustness of our findings.
Our analysis revealed a significant causal relationship between genetic predisposition to UC and increased susceptibility to DKD. Specifically, individuals with a genetic susceptibility to UC exhibited a 17.3% higher risk of developing DKD. However, we found no evidence of a causal link between DKD and the risk of developing UC. Additionally, we identified shared genetic risk factors and molecular pathways linking UC and DKD, thereby highlighting potential therapeutic targets.
This study underscores the intricate genetic interplay between UC and DKD, suggesting that individuals with UC may be at an elevated risk for developing DKD. Understanding these shared genetic pathways could facilitate the development of early detection strategies and targeted interventions for individuals at risk of DKD. Ultimately, these insights could lead to improved clinical outcomes for patients suffering from both conditions.</abstract><cop>Switzerland</cop><pub>Frontiers Media S.A</pub><pmid>39211444</pmid><doi>10.3389/fendo.2024.1435812</doi><oa>free_for_read</oa></addata></record> |
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subjects | Colitis, Ulcerative - complications Colitis, Ulcerative - genetics diabetic kidney disease Diabetic Nephropathies - genetics Endocrinology genetic causality Genetic Predisposition to Disease genome-wide association studies (GWAS) Genome-Wide Association Study Humans Mendelian randomization Mendelian Randomization Analysis Polymorphism, Single Nucleotide Risk Factors ulcerative colitis |
title | Elucidating the genetic relationship between ulcerative colitis and diabetic kidney disease: a bidirectional Mendelian randomization study |
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