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Article: Impact of periodontitis on type 2 diabetes: a bioinformatic analysis

TitleImpact of periodontitis on type 2 diabetes: a bioinformatic analysis
Authors
KeywordsGenome-wide association study
Mendelian randomization
Periodontitis
Single cell analysis
Type 2 diabetes
Issue Date29-May-2024
PublisherBioMed Central
Citation
BMC Oral Health, 2024, v. 24, n. 1 How to Cite?
AbstractBackground: Periodontitis is strongly associated with type 2 diabetes (T2D) that results in serious complications and mortality. However, the pathogenic role of periodontitis in the development of T2D and the underlain mechanism have not been fully elucidated. Methods: A Mendelian randomization (MR) was performed to estimate the causality between two diseases. Bioinformatics tools, including gene ontology and pathway enrichment analyses, were employed to analyze the common differentially expressed genes (DEGs) in periodontitis and T2D. MR and colocalization analyses were then utilized to investigate the causal associations between potential pathogenic gene expression and the risk of T2D. Single cell-type expression analysis was further performed to detect the cellular localization of these genes. Results: Genetically predicted periodontitis was associated with a higher risk of T2D (OR, 1.469; 95% CI, 1.117–1.930; P = 0.006) and insulin resistance (OR 1.034; 95%CI 1.001–1.068; P = 0.041). 79 common DEGs associated with periodontitis and T2D were then identified and demonstrated enrichment mainly in CXC receptor chemokine receptor binding and interleutin-17 signaling pathway. The integration of GWAS with the expression quantitative trait locis of these genes from the peripheral blood genetically prioritized 6 candidate genes, including 2 risk genes (RAP2A, MCUR1) and 4 protective genes (WNK1, NFIX, FOS, PANX1) in periodontitis-related T2D. Enriched in natural killer cells, RAP2A (OR 4.909; 95% CI 1.849–13.039; P = 0.001) demonstrated high risk influence on T2D, and exhibited strong genetic evidence of colocalization (coloc.abf-PPH4 = 0.632). Conclusions: This study used a multi-omics integration method to explore causality between periodontitis and T2D, and revealed molecular mechanisms using bioinformatics tools. Periodontitis was associated with a higher risk of T2D. MCUR1, RAP2A, FOS, PANX1, NFIX and WNK1 may play important roles in the pathogenesis of periodontitis-related T2D, shedding light on the development of potential drug targets.
Persistent Identifierhttp://hdl.handle.net/10722/347960
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 0.737

 

DC FieldValueLanguage
dc.contributor.authorWei, Xindi-
dc.contributor.authorZhang, Xiaomeng-
dc.contributor.authorChen, Ruiying-
dc.contributor.authorLi, Yuan-
dc.contributor.authorYang, Yijie-
dc.contributor.authorDeng, Ke-
dc.contributor.authorCai, Zhengzhen-
dc.contributor.authorLai, Hongchang-
dc.contributor.authorShi, Junyu-
dc.date.accessioned2024-10-03T00:30:45Z-
dc.date.available2024-10-03T00:30:45Z-
dc.date.issued2024-05-29-
dc.identifier.citationBMC Oral Health, 2024, v. 24, n. 1-
dc.identifier.issn1472-6831-
dc.identifier.urihttp://hdl.handle.net/10722/347960-
dc.description.abstractBackground: Periodontitis is strongly associated with type 2 diabetes (T2D) that results in serious complications and mortality. However, the pathogenic role of periodontitis in the development of T2D and the underlain mechanism have not been fully elucidated. Methods: A Mendelian randomization (MR) was performed to estimate the causality between two diseases. Bioinformatics tools, including gene ontology and pathway enrichment analyses, were employed to analyze the common differentially expressed genes (DEGs) in periodontitis and T2D. MR and colocalization analyses were then utilized to investigate the causal associations between potential pathogenic gene expression and the risk of T2D. Single cell-type expression analysis was further performed to detect the cellular localization of these genes. Results: Genetically predicted periodontitis was associated with a higher risk of T2D (OR, 1.469; 95% CI, 1.117–1.930; P = 0.006) and insulin resistance (OR 1.034; 95%CI 1.001–1.068; P = 0.041). 79 common DEGs associated with periodontitis and T2D were then identified and demonstrated enrichment mainly in CXC receptor chemokine receptor binding and interleutin-17 signaling pathway. The integration of GWAS with the expression quantitative trait locis of these genes from the peripheral blood genetically prioritized 6 candidate genes, including 2 risk genes (RAP2A, MCUR1) and 4 protective genes (WNK1, NFIX, FOS, PANX1) in periodontitis-related T2D. Enriched in natural killer cells, RAP2A (OR 4.909; 95% CI 1.849–13.039; P = 0.001) demonstrated high risk influence on T2D, and exhibited strong genetic evidence of colocalization (coloc.abf-PPH4 = 0.632). Conclusions: This study used a multi-omics integration method to explore causality between periodontitis and T2D, and revealed molecular mechanisms using bioinformatics tools. Periodontitis was associated with a higher risk of T2D. MCUR1, RAP2A, FOS, PANX1, NFIX and WNK1 may play important roles in the pathogenesis of periodontitis-related T2D, shedding light on the development of potential drug targets.-
dc.languageeng-
dc.publisherBioMed Central-
dc.relation.ispartofBMC Oral Health-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectGenome-wide association study-
dc.subjectMendelian randomization-
dc.subjectPeriodontitis-
dc.subjectSingle cell analysis-
dc.subjectType 2 diabetes-
dc.titleImpact of periodontitis on type 2 diabetes: a bioinformatic analysis-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/s12903-024-04408-1-
dc.identifier.scopuseid_2-s2.0-85194885356-
dc.identifier.volume24-
dc.identifier.issue1-
dc.identifier.eissn1472-6831-
dc.identifier.issnl1472-6831-

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