{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T11:09:06Z","timestamp":1791544146101,"version":"4.3.4"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2022,5,18]],"date-time":"2022-05-18T00:00:00Z","timestamp":1652832000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/ http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Aims:<\/jats:title>\n                    <jats:p>There is an ongoing debate on whether NAFLD is an active contributor or an innocent bystander in the pathogenesis of coronary artery disease (CAD). The aim of the present study was to assess the causal relationship between NAFLD and CAD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results:<\/jats:title>\n                    <jats:p>We performed two\u2010sample Mendelian randomization (MR) analyses using summary\u2010level data to assess the association between genetically predicted NAFLD (i.e., chronically elevated serum alanine aminotransferase levels [cALT], imaging\u2010based and biopsy\u2010confirmed NAFLD) and risk of CAD. Analyses were repeated after exclusion of NAFLD susceptibility genes that are associated with impaired VLDL secretion.<\/jats:p>\n                    <jats:p>Inverse\u2010variance weighted MR analyses showed a statistically significant association between genetically predicted cALT and risk of CAD (OR: 1.116, 95% CI: 1.039, 1.199), but not for the other NAFLD\u2010related traits (OR: 1.046, 95% CI: 0.764, 1.433 and OR: 1.014, 95% CI: 0.968, 1.062 for imaging\u2010based and biopsy\u2010confirmed NAFLD, respectively). MR\u2010Egger regression revealed a statistically significant intercept, indicative of directional pleiotropy, for all traits. Repeat analyses after exclusion of genes associated with impaired VLDL secretion showed consistent associations between genetically predicted NAFLD and CAD for all traits (i.e., cALT [OR: 1.203, 95% CI: 1.113, 1.300]), imaging\u2010based (OR: 2.149, 95% CI: 1.276, 3.620) and biopsy\u2010confirmed NAFLD (OR: 1.113, 95% CI: 1.041, 1.189), which persisted when more stringent biopsy\u2010confirmed NAFLD criteria were used (OR: 1.154, 95% CI: 1.043, 1.278) or when more stringent MR methods were applied. MR\u2010Egger regression did not show a statistically significant intercept.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>The two\u2010sample MR analyses showed a robust association between genetically predicted NAFLD and CAD after exclusion of genetic variants that are implicated in impaired VLDL secretion.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.32534","type":"journal-article","created":{"date-parts":[[2022,4,20]],"date-time":"2022-04-20T05:48:46Z","timestamp":1650433726000},"page":"230-238","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":112,"title":["Relationship between NAFLD and coronary artery disease: A Mendelian randomization study"],"prefix":"10.1097","volume":"77","author":[{"given":"Zhewen","family":"Ren","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Metabolic Diseases, Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands"},{"name":"5211,Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands"},{"name":"5211,CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pomme I. H. G.","family":"Simons","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolic Diseases, Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands"},{"name":"5211,Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands"},{"name":"5211,CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anke","family":"Wesselius","sequence":"additional","affiliation":[{"name":"5211,NUTRIM School for Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands"},{"name":"5211,Department of Epidemiology, Maastricht University, Maastricht, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Coen D. A.","family":"Stehouwer","sequence":"additional","affiliation":[{"name":"5211,Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands"},{"name":"5211,CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands"},{"name":"Division of General Internal Medicine, Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8229-3331","authenticated-orcid":false,"given":"Martijn C. G. J.","family":"Brouwers","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolic Diseases, Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands"},{"name":"5211,CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2022,5,18]]},"reference":[{"key":"R1-20260413","doi-asserted-by":"crossref","first-page":"73","DOI":"10.1002\/hep.28431","article-title":"Global epidemiology of nonalcoholic fatty liver disease\u2014meta\u2010analytic assessment of prevalence, incidence, and outcomes","volume":"64","year":"2016","journal-title":"Hepatology"},{"key":"R2-20260413","doi-asserted-by":"crossref","first-page":"1388","DOI":"10.1016\/j.jhep.2015.11.004","article-title":"EASL\u2010EASD\u2010EASO Clinical Practice Guidelines for the management of non\u2010alcoholic fatty liver 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