PURPOSE OF REVIEW: To evaluate whether new and known genetic determinants of plasma levels of LDL cholesterol, lipoprotein(a), triglyceride-rich lipoproteins, and HDL cholesterol associate with the risk of cardiovascular disease expected from the effect on lipoprotein levels. Concordance or discordance of such genetic determinants with cardiovascular disease risk will either favor or disfavor that these lipoproteins are causally related to cardiovascular disease. RECENT FINDINGS: Evidence for concordance or discordance with cardiovascular disease risk has come from Mendelian randomization studies, whereas indirect evidence also has emerged from genome-wide and candidate gene association studies. The major limitations of studies of genetic variation and concordance or discordance with cardiovascular disease are pleiotropic effects of the variants studied, and/or lack of sufficient statistical power of the majority of studies to firmly demonstrate a positive association, or even more difficult, to exclude an association. SUMMARY: New and known genetic determinants of plasma levels of LDL cholesterol, lipoprotein(a), and triglyceride-rich lipoproteins are concordant with both the magnitude and direction of the expected risk of cardiovascular disease, whereas this is unclear for HDL cholesterol. The data are compatible with cardiovascular disease causality for the three former lipoprotein classes, but not for HDL cholesterol.
PURPOSE OF REVIEW: To evaluate whether new and known genetic determinants of plasma levels of LDL cholesterol, lipoprotein(a), triglyceride-rich lipoproteins, and HDL cholesterol associate with the risk of cardiovascular disease expected from the effect on lipoprotein levels. Concordance or discordance of such genetic determinants with cardiovascular disease risk will either favor or disfavor that these lipoproteins are causally related to cardiovascular disease. RECENT FINDINGS: Evidence for concordance or discordance with cardiovascular disease risk has come from Mendelian randomization studies, whereas indirect evidence also has emerged from genome-wide and candidate gene association studies. The major limitations of studies of genetic variation and concordance or discordance with cardiovascular disease are pleiotropic effects of the variants studied, and/or lack of sufficient statistical power of the majority of studies to firmly demonstrate a positive association, or even more difficult, to exclude an association. SUMMARY: New and known genetic determinants of plasma levels of LDL cholesterol, lipoprotein(a), and triglyceride-rich lipoproteins are concordant with both the magnitude and direction of the expected risk of cardiovascular disease, whereas this is unclear for HDL cholesterol. The data are compatible with cardiovascular disease causality for the three former lipoprotein classes, but not for HDL cholesterol.
Authors: Brian H Shirts; Michael T Howard; Sandra J Hasstedt; M Nazeem Nanjee; Stacey Knight; John F Carlquist; Jeffrey L Anderson; Paul N Hopkins; Steven C Hunt Journal: Atherosclerosis Date: 2012-03-01 Impact factor: 5.162
Authors: Jenny Sandmark; Anna Tigerström; Tomas Akerud; Magnus Althage; Thomas Antonsson; Stefan Blaho; Cristian Bodin; Jonas Boström; Yantao Chen; Anders Dahlén; Per-Olof Eriksson; Emma Evertsson; Tomas Fex; Ola Fjellström; David Gustafsson; Margareta Herslöf; Ryan Hicks; Emelie Jarkvist; Carina Johansson; Inge Kalies; Birgitta Karlsson Svalstedt; Fredrik Kartberg; Anne Legnehed; Sofia Martinsson; Andreas Moberg; Marianne Ridderström; Birgitta Rosengren; Alan Sabirsh; Anders Thelin; Johanna Vinblad; Annika U Wellner; Bingze Xu; Ann-Margret Östlund-Lindqvist; Wolfgang Knecht Journal: J Biol Chem Date: 2020-03-04 Impact factor: 5.157
Authors: Katariina Öörni; Kristiina Rajamäki; Su Duy Nguyen; Katariina Lähdesmäki; Riia Plihtari; Miriam Lee-Rueckert; Petri T Kovanen Journal: J Lipid Res Date: 2014-11-25 Impact factor: 5.922