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<jats:title>Objective<\/jats:title>\n                    <jats:p>In this study, we aimed to establish the causal effects of lowering sclerostin, target of the antiosteoporosis drug romosozumab, on atherosclerosis and its risk factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A genome\u2010wide association study meta\u2010analysis was performed of circulating sclerostin levels in 33,961 European individuals. Mendelian randomization (MR) was used to predict the causal effects of sclerostin lowering on 15 atherosclerosis\u2010related diseases and risk factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found that 18 conditionally independent variants were associated with circulating sclerostin. Of these, 1\n                      <jats:italic>cis<\/jats:italic>\n                      signal in\n                      <jats:italic>SOST<\/jats:italic>\n                      and 3\n                      <jats:italic>trans<\/jats:italic>\n                      signals in\n                      <jats:italic>B4GALNT3<\/jats:italic>\n                      ,\n                      <jats:italic>RIN3<\/jats:italic>\n                      , and\n                      <jats:italic>SERPINA1<\/jats:italic>\n                      regions showed directionally opposite signals for sclerostin levels and estimated bone mineral density. Variants with these 4 regions were selected as genetic instruments. MR using 5 correlated\n                      <jats:italic>cis<\/jats:italic>\n                      \u2010SNPs suggested that lower sclerostin increased the risk of type 2 diabetes mellitus (DM) (odds ratio [OR] 1.32 [95% confidence interval (95% CI) 1.03\u20131.69]) and myocardial infarction (MI) (OR 1.35 [95% CI 1.01\u20131.79]); sclerostin lowering was also suggested to increase the extent of coronary artery calcification (CAC) (\u03b2\u00a0=\u00a00.24 [95% CI 0.02\u20130.45]). MR using both\n                      <jats:italic>cis<\/jats:italic>\n                      and\n                      <jats:italic>trans<\/jats:italic>\n                      instruments suggested that lower sclerostin increased hypertension risk (OR 1.09 [95% CI 1.04\u20131.15]), but otherwise had attenuated effects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study provides genetic evidence to suggest that lower levels of sclerostin may increase the risk of hypertension, type 2 DM, MI, and the extent of CAC. Taken together, these findings underscore the requirement for strategies to mitigate potential adverse effects of romosozumab treatment on atherosclerosis and its related risk factors.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art42538-toc-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.42538","type":"journal-article","created":{"date-parts":[[2023,4,25]],"date-time":"2023-04-25T04:14:15Z","timestamp":1682396055000},"page":"1781-1792","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Lowering of Circulating Sclerostin May Increase Risk of Atherosclerosis and Its Risk Factors: Evidence From a\n                    <scp>Genome\u2010Wide<\/scp>\n                    Association\n                    <scp>Meta\u2010Analysis<\/scp>\n                    Followed by Mendelian Randomization"],"prefix":"10.1002","volume":"75","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6623-6839","authenticated-orcid":false,"given":"Jie","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China, and Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the People's Republic of China, Shanghai Key Laboratory for Endocrine Tumor, State Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiao Tong..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleanor","family":"Wheeler","sequence":"additional","affiliation":[{"name":"MRC Epidemiology Unit, Institute of Metabolic Science University of Cambridge School of Clinical Medicine  Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maik","family":"Pietzner","sequence":"additional","affiliation":[{"name":"MRC Epidemiology Unit, Institute of Metabolic Science, University of Cambridge School of Clinical Medicine, Cambridge, UK, and Computational Medicine, Berlin Institute of Health at Charit\u00e9\u2013Universit\u00e4tsmedizin Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Till F. 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