APOE gene variants in primary dyslipidemia

被引:97
作者
Abou Khalil, Yara [1 ,2 ,3 ]
Rabes, Jean-Pierre [1 ,4 ,5 ]
Boileau, Catherine [1 ,2 ,6 ]
Varret, Mathilde [1 ,2 ]
机构
[1] Ctr Hosp Univ Xavier Bichat, Lab Vasc Translat Sci LVTS, INSERM U1148, Paris, France
[2] Univ Paris, Paris, France
[3] St Joseph Univ, Lab Biochem & Mol Therapeut LBTM, Pole Technol Sante PTS, Fac Pharm, Beirut, Lebanon
[4] Paris Saclay, Ctr Hosp Univ Ambroise Pare, AP HP, Lab Biochem & Mol Genet,HUPIFO, Boulogne, France
[5] UVSQ, UFR Simone Veil Sante, Montigny Le Bretonneux, France
[6] CHU Xavier Bichat, AP HP, Genet Dept, Paris, France
关键词
APOE; Genetic variants; Familial hypercholesterolemia; Autosomal dominant; Hypercholesterolemia; Familial combined hyperlipidemia; Dysbetalipoproteinemia; Lipoprotein glomerulopathy; APOLIPOPROTEIN-E MUTATION; AUTOSOMAL-DOMINANT HYPERCHOLESTEROLEMIA; III HYPERLIPOPROTEINEMIA; FAMILIAL HYPERCHOLESTEROLEMIA; LIPOPROTEIN GLOMERULOPATHY; P.LEU167DEL MUTATION; CLINICAL-DIAGNOSIS; NEPHROTIC SYNDROME; MOLECULAR-BASIS; ACID DELETION;
D O I
10.1016/j.atherosclerosis.2021.05.007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Apolipoprotein E (apoE) is a major apolipoprotein involved in lipoprotein metabolism. It is a polymorphic protein and different isoforms are associated with variations in lipid and lipoprotein levels and thus cardiovascular risk. The isoform apoE4 is associated with an increase in LDL-cholesterol levels and thus a higher cardiovascular risk compared to apoE3. Whereas, apoE2 is associated with a mild decrease in LDL-cholesterol levels. In the presence of other risk factors, apoE2 homozygotes could develop type III hyperlipoproteinemia (familial dysbetalipoproteinemia or FD), an atherogenic disorder characterized by an accumulation of remnants of triglyceride-rich lipoproteins. Several rare APOE gene variants were reported in different types of dyslipidemias including FD, familial combined hyperlipidemia (FCH), lipoprotein glomerulopathy and bona fide autosomal dominant hypercholesterolemia (ADH). ADH is characterized by elevated LDL-cholesterol levels leading to coronary heart disease, and due to molecular alterations in three main genes: LDLR, APOB and PCSK9. The identification of the APOE-p.Leu167del variant as the causative molecular element in two different ADH families, paved the way to considering APOE as a candidate gene for ADH. Due to non mendelian interacting factors, common genetic and environmental factors and perhaps epigenetics, clinical presentation of lipid disorders associated with APOE variants often strongly overlap. More studies are needed to determine the spectrum of APOE implication in each of the diseases, notably ADH, in order to improve clinical and genetic diagnosis, prognosis and patient management. The purpose of this review is to comment on these APOE variants and on the molecular and clinical overlaps between dyslipidemias.
引用
收藏
页码:11 / 22
页数:12
相关论文
共 127 条
[11]   PCSK9: from biology to clinical applications [J].
Blanchard, Valentin ;
Khantalin, Ilya ;
Ramin-Mangata, Stephane ;
Chemello, Kevin ;
Nativel, Brice ;
Lambert, Gilles .
PATHOLOGY, 2019, 51 (02) :177-183
[12]   Kinetics of plasma apolipoprotein E isoforms by LC-MS/MS: a pilot study [J].
Blanchard, Valentin ;
Ramin-Mangata, Stephane ;
Billon-Crossouard, Stephanie ;
Aguesse, Audrey ;
Durand, Manon ;
Chemello, Kevin ;
Nativel, Brice ;
Flet, Laurent ;
Chetiveaux, Maud ;
Jacobi, David ;
Bard, Jean-Marie ;
Ouguerram, Khadija ;
Lambert, Gilles ;
Krempf, Michel ;
Croyal, Mikael .
JOURNAL OF LIPID RESEARCH, 2018, 59 (05) :892-900
[13]   A new apolipoprotein E mutation, apoE Las Vegas, in a European-American with lipoprotein glomerulopathy [J].
Bomback, Andrew S. ;
Song, Huijuan ;
D'Agati, Vivette D. ;
Cohen, Scott D. ;
Neal, Alison ;
Appel, Gerald B. ;
Rovin, Brad H. .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2010, 25 (10) :3442-3446
[14]   Comparison of Plasma Lipoprotein Composition and Function in Cerebral Amyloid Angiopathy and Alzheimer's Disease [J].
Bonaterra-Pastra, Anna ;
Fernandez-de-Retana, Sofia ;
Rivas-Urbina, Andrea ;
Puig, Nuria ;
Benitez, Sonia ;
Pancorbo, Olalla ;
Rodriguez-Luna, David ;
Pujadas, Francesc ;
del Mar Freijo, Maria ;
Tur, Silvia ;
Martinez-Zabaleta, Maite ;
Cardona Portela, Pere ;
Vera, Rocio ;
Lebrato-Hernandez, Lucia ;
Arenillas, Juan F. ;
Perez-Sanchez, Soledad ;
Montaner, Joan ;
Sanchez-Quesada, Jose Luis ;
Hernandez-Guillamon, Mar .
BIOMEDICINES, 2021, 9 (01) :1-14
[15]   The genetics of familial combined hyperlipidaemia [J].
Brouwers, Martijn C. G. J. ;
van Greevenbroek, Marleen M. J. ;
Stehouwer, Coen D. A. ;
de Graaf, Jacqueline ;
Stalenhoef, Anton F. H. .
NATURE REVIEWS ENDOCRINOLOGY, 2012, 8 (06) :352-362
[16]   Novel Genetic Mutation in Apolipoprotein E2 Homozygosis and Its Implication in Organ Donation: A Case Report [J].
Cautero, N. ;
Di Benedetto, F. ;
De Ruvo, N. ;
Montalti, R. ;
Guerrini, G. P. ;
Ballarin, R. ;
Spaggiari, M. ;
Smerieri, N. ;
De Blasiis, M. G. ;
Rompianesi, G. ;
Iemmolo, R. M. ;
Marino, M. ;
Bertolotti, M. ;
Zivieri, S. ;
Gerunda, G. E. .
TRANSPLANTATION PROCEEDINGS, 2010, 42 (04) :1349-1351
[17]   A presumptive new locus for autosomal dominant hypercholesterolemia mapping to 8q24.22 [J].
Cenarro, A. ;
Garcia-Otin, A-L ;
Tejedor, M. T. ;
Solanas, M. ;
Jarauta, E. ;
Junquera, C. ;
Ros, E. ;
Mozas, P. ;
Puzo, J. ;
Pocovi, M. ;
Civeira, F. .
CLINICAL GENETICS, 2011, 79 (05) :475-481
[18]   The p.Leu167del Mutation in APOE Gene Causes Autosomal Dominant Hypercholesterolemia by Down-regulation of LDL Receptor Expression in Hepatocytes [J].
Cenarro, Ana ;
Etxebarria, Aitor ;
de Castro-Oros, Isabel ;
Stef, Marianne ;
Bea, Ana M. ;
Palacios, Lourdes ;
Mateo-Gallego, Rocio ;
Benito-Vicente, Asier ;
Ostolaza, Helena ;
Tejedor, Teresa ;
Martin, Cesar ;
Civeira, Fernando .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2016, 101 (05) :2113-2121
[19]  
Cheung C. Y., 2009, Hong Kong Medical Journal, V15, P57
[20]   Apo E variants in patients with type III hyperlipoproteinemia [J].
Civeira, F ;
Pocovi, M ;
Cenarro, A ;
Casao, E ;
Vilella, E ;
Joven, J ;
Gonzalez, J ;
GarciaOtin, AL ;
Ordovas, JM .
ATHEROSCLEROSIS, 1996, 127 (02) :273-282