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Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study

OBJECTIVES: Heart failure (HF) has been implicated in osteoporosis. However, causality remains unestablished. Here, we sought to assess causal associations of genetic liability to HF with osteoporosis using Mendelian randomization (MR) analyses. METHODS: Independent single nucleotide polymorphisms a...

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Autores principales: Chen, Heng, Ye, Runze, Guo, Xiaogang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9636651/
https://www.ncbi.nlm.nih.gov/pubmed/36333784
http://dx.doi.org/10.1186/s12920-022-01385-8
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author Chen, Heng
Ye, Runze
Guo, Xiaogang
author_facet Chen, Heng
Ye, Runze
Guo, Xiaogang
author_sort Chen, Heng
collection PubMed
description OBJECTIVES: Heart failure (HF) has been implicated in osteoporosis. However, causality remains unestablished. Here, we sought to assess causal associations of genetic liability to HF with osteoporosis using Mendelian randomization (MR) analyses. METHODS: Independent single nucleotide polymorphisms associated with HF at genome-wide significance were derived from a large genome-wide association study (GWAS) (including up to 977,323 individuals). We obtained summary statistics for forearm (FA) bone mineral density (BMD) (n = 8,143), femoral neck (FN) BMD (n = 32,735), lumbar spine (LS) BMD (n = 28,498), heel (HE) BMD (n = 426,824), and fracture (n = 1,214,434) from other GWAS meta-analyses. Inverse variance weighted (IVW) and several supplementary methods were performed to calculate the MR estimates. RESULTS: Genetically determined HF has no causal effect on FA-BMD (odds ratio (OR) 1.17; 95% confidence interval (CI) 0.82, 1.66; P = 0.389), FN-BMD (OR 1.01; 95% CI 0.85, 1.19; P = 0.936), LS-BMD (OR 0.96; 95% CI 0.80, 1.17; P = 0.705), HE-BMD (OR 1.01; 95% CI 0.90, 1.13; P = 0.884), and fracture risk (OR 1.00; 95% CI 0.92, 1.10; P = 0.927). Complementary analyses returned broadly consistent results. CONCLUSION: This MR study provides genetic evidence that HF may not lead to an increased risk of reduced BMDs or fracture. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12920-022-01385-8.
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spelling pubmed-96366512022-11-06 Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study Chen, Heng Ye, Runze Guo, Xiaogang BMC Med Genomics Research OBJECTIVES: Heart failure (HF) has been implicated in osteoporosis. However, causality remains unestablished. Here, we sought to assess causal associations of genetic liability to HF with osteoporosis using Mendelian randomization (MR) analyses. METHODS: Independent single nucleotide polymorphisms associated with HF at genome-wide significance were derived from a large genome-wide association study (GWAS) (including up to 977,323 individuals). We obtained summary statistics for forearm (FA) bone mineral density (BMD) (n = 8,143), femoral neck (FN) BMD (n = 32,735), lumbar spine (LS) BMD (n = 28,498), heel (HE) BMD (n = 426,824), and fracture (n = 1,214,434) from other GWAS meta-analyses. Inverse variance weighted (IVW) and several supplementary methods were performed to calculate the MR estimates. RESULTS: Genetically determined HF has no causal effect on FA-BMD (odds ratio (OR) 1.17; 95% confidence interval (CI) 0.82, 1.66; P = 0.389), FN-BMD (OR 1.01; 95% CI 0.85, 1.19; P = 0.936), LS-BMD (OR 0.96; 95% CI 0.80, 1.17; P = 0.705), HE-BMD (OR 1.01; 95% CI 0.90, 1.13; P = 0.884), and fracture risk (OR 1.00; 95% CI 0.92, 1.10; P = 0.927). Complementary analyses returned broadly consistent results. CONCLUSION: This MR study provides genetic evidence that HF may not lead to an increased risk of reduced BMDs or fracture. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12920-022-01385-8. BioMed Central 2022-11-04 /pmc/articles/PMC9636651/ /pubmed/36333784 http://dx.doi.org/10.1186/s12920-022-01385-8 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Chen, Heng
Ye, Runze
Guo, Xiaogang
Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study
title Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study
title_full Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study
title_fullStr Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study
title_full_unstemmed Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study
title_short Lack of causal association between heart failure and osteoporosis: a Mendelian randomization study
title_sort lack of causal association between heart failure and osteoporosis: a mendelian randomization study
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9636651/
https://www.ncbi.nlm.nih.gov/pubmed/36333784
http://dx.doi.org/10.1186/s12920-022-01385-8
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