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      Peripheral Inflammatory Factors and Acute Myocardial Infarction Risk: A Mendelian Randomization Study

      research-article
      1 , 2 , 1 , 2
      Global Heart
      Ubiquity Press
      Inflammation, Interleukin-10, Interleukin-18, Mendelian randomization, Myocardial infarction

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          Abstract

          Background:

          Previous observational studies have confirmed the relationship between inflammation and acute myocardial infarction (AMI), but genetic evidence is still lacking. The aim of this study was to explore the bidirectional association of multiple peripheral inflammatory factors with this disease at the genetic level.

          Methods:

          Summary data for AMI and several peripheral inflammatory factors (such as interleukin-10 and interleukin-18) were collected from published genome-wide correlation studies. Based on the correlation, independence, and exclusivity assumptions, a total of 9 to 110 instrumental variables were selected from these summary data to predict the above traits. Two-sample Mendelian randomization methods, including inverse-variance weighted (IVW), were used to make causal inferences between exposures and outcomes. Sensitivity analyses including Cochran’s Q, MR-Egger intercept, leave-one-out, forest plot, and MR-PRESSO were adopted to assess heterogeneity and horizontal pleiotropy.

          Results:

          The IVW reported that elevated peripheral levels of interleukin-10 and interleukin-18 were nominally associated with a reduced risk of AMI (OR = 0.876, 95% CI = 0.788 ~ 0.974, P = 0.015; OR = 0.934, 95% CI = 0.875 ~ 0.997, P = 0.040). The IVW also reported that the risk of AMI nominally increased the peripheral level of interleukin-10 (OR = 1.062, 95% CI = 1.003 ~ 1.124, P = 0.040). No significant heterogeneity or horizontal pleiotropy were found by sensitivity analyses.

          Conclusion:

          Both interleukin-10 and interleukin-18 were peripheral inflammatory factors genetically associated with AMI. In particular, combined with previous knowledge, interleukin-10 may have a protective effect on the onset, progression, and prognosis of the disease.

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          Most cited references34

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          Mendelian Randomization.

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            MendelianRandomization: an R package for performing Mendelian randomization analyses using summarized data

            Abstract MendelianRandomization is a software package for the R open-source software environment that performs Mendelian randomization analyses using summarized data. The core functionality is to implement the inverse-variance weighted, MR-Egger and weighted median methods for multiple genetic variants. Several options are available to the user, such as the use of robust regression, fixed- or random-effects models and the penalization of weights for genetic variants with heterogeneous causal estimates. Extensions to these methods, such as allowing for variants to be correlated, can be chosen if appropriate. Graphical commands allow summarized data to be displayed in an interactive graph, or the plotting of causal estimates from multiple methods, for comparison. Although the main method of data entry is directly by the user, there is also an option for allowing summarized data to be incorporated from the PhenoScanner database of genotype—phenotype associations. We hope to develop this feature in future versions of the package. The R software environment is available for download from [https://www.r-project.org/]. The MendelianRandomization package can be downloaded from the Comprehensive R Archive Network (CRAN) within R, or directly from [https://cran.r-project.org/web/packages/MendelianRandomization/]. Both R and the MendelianRandomization package are released under GNU General Public Licenses (GPL-2|GPL-3).
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              Genomic atlas of the human plasma proteome

              Although plasma proteins have important roles in biological processes and are the direct targets of many drugs, the genetic factors that control inter-individual variation in plasma protein levels are not well understood. Here we characterize the genetic architecture of the human plasma proteome in healthy blood donors from the INTERVAL study. We identify 1,927 genetic associations with 1,478 proteins, a fourfold increase on existing knowledge, including trans associations for 1,104 proteins. To understand the consequences of perturbations in plasma protein levels, we apply an integrated approach that links genetic variation with biological pathway, disease, and drug databases. We show that protein quantitative trait loci overlap with gene expression quantitative trait loci, as well as with disease-associated loci, and find evidence that protein biomarkers have causal roles in disease using Mendelian randomization analysis. By linking genetic factors to diseases via specific proteins, our analyses highlight potential therapeutic targets, opportunities for matching existing drugs with new disease indications, and potential safety concerns for drugs under development.
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                Author and article information

                Contributors
                Journal
                Glob Heart
                Glob Heart
                2211-8179
                Global Heart
                Ubiquity Press
                2211-8160
                2211-8179
                06 October 2023
                2023
                : 18
                : 1
                : 55
                Affiliations
                [1 ]Department of Critical Care Medicine, West China Hospital, Sichuan University, China
                [2 ]West China School of Nursing, Sichuan University, Chengdu 610000, Sichuan Province, China
                Author notes
                CORRESPONDING AUTHOR: Ling Zeng Department of Critical Care Medicine, West China Hospital, Sichuan University; West China School of Nursing, Sichuan University; No. 37, Guoxue Road, Wuhou District, Chengdu 610000, Sichuan Province, China zengling346789@ 123456outlook.com
                Article
                10.5334/gh.1269
                10558024
                37811136
                1516b12d-1a67-4b30-8a5b-8b50b8e275f7
                Copyright: © 2023 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC-BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See http://creativecommons.org/licenses/by/4.0/.

                History
                : 05 May 2023
                : 05 September 2023
                Categories
                Original Research

                inflammation,interleukin-10,interleukin-18,mendelian randomization,myocardial infarction

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