Familial Hypercholesterolemia: The Most Frequent Cholesterol Metabolism Disorder Caused Disease

被引:99
作者
Benito-Vicente, Asier [1 ]
Uribe, Kepa B. [1 ]
Jebari, Shifa [1 ]
Galicia-Garcia, Unai [1 ]
Ostolaza, Helena [1 ]
Martin, Cesar [1 ]
机构
[1] Univ Basque Country, Dept Bioquim, Inst Biofis, UPV EHU,CSIC, Apdo 644, E-48080 Bilbao, Spain
关键词
cholesterol; metabolism; familial hypercholesterolemia; DENSITY-LIPOPROTEIN-RECEPTOR; STEROL-SENSING DOMAIN; APO-B MUTATIONS; LDL RECEPTOR; FUNCTIONAL-CHARACTERIZATION; INTRACELLULAR TRAFFICKING; CHYLOMICRON UPTAKE; ABCA1; EXPRESSION; EGF-A; PCSK9;
D O I
10.3390/ijms19113426
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cholesterol is an essential component of cell barrier formation and signaling transduction involved in many essential physiologic processes. For this reason, cholesterol metabolism must be tightly controlled. Cell cholesterol is mainly acquired from two sources: Dietary cholesterol, which is absorbed in the intestine and, intracellularly synthesized cholesterol that is mainly synthesized in the liver. Once acquired, both are delivered to peripheral tissues in a lipoprotein dependent mechanism. Malfunctioning of cholesterol metabolism is caused by multiple hereditary diseases, including Familial Hypercholesterolemia, Sitosterolemia Type C and Niemann-Pick Type C1. Of these, familial hypercholesterolemia (FH) is a common inherited autosomal co-dominant disorder characterized by high plasma cholesterol levels. Its frequency is estimated to be 1:200 and, if untreated, increases the risk of premature cardiovascular disease. This review aims to summarize the current knowledge on cholesterol metabolism and the relation of FH to cholesterol homeostasis with special focus on the genetics, diagnosis and treatment.
引用
收藏
页数:21
相关论文
共 158 条
[1]   Mutations in PCSK9 cause autosomal dominant hypercholesterolemia [J].
Abifadel, M ;
Varret, M ;
Rabès, JP ;
Allard, D ;
Ouguerram, K ;
Devillers, M ;
Cruaud, C ;
Benjannet, S ;
Wickham, L ;
Erlich, D ;
Derré, A ;
Villéger, L ;
Farnier, M ;
Beucler, I ;
Bruckert, E ;
Chambaz, J ;
Chanu, B ;
Lecerf, JM ;
Luc, G ;
Moulin, P ;
Weissenbach, J ;
Prat, A ;
Krempf, M ;
Junien, C ;
Seidah, NG ;
Boileau, C .
NATURE GENETICS, 2003, 34 (02) :154-156
[2]  
Agrawal S, 2018, NAT REV NEPHROL, V14, P57, DOI 10.1038/nrneph.2017.155
[3]   Niemann-Pick C1 like 1 protein is critical for intestinal cholesterol absorption [J].
Altmann, SW ;
Davis, HR ;
Zhu, LJ ;
Yao, XR ;
Hoos, LM ;
Tetzloff, G ;
Iyer, SPN ;
Maguire, M ;
Golovko, A ;
Zeng, M ;
Wang, LQ ;
Murgolo, N ;
Graziano, MP .
SCIENCE, 2004, 303 (5661) :1201-1204
[4]   MicroRNA-27a decreases the level and efficiency of the LDL receptor and contributes to the dysregulation of cholesterol homeostasis [J].
Alvarez, M. Lucrecia ;
Khosroheidari, Mahdieh ;
Eddy, Elena ;
Done, Stefania C. .
ATHEROSCLEROSIS, 2015, 242 (02) :595-604
[5]   Further evidence of novel APOB mutations as a cause of familial hypercholesterolaemia [J].
Alves, Ana Catarina ;
Benito-Vicente, Asier ;
Medeiros, Ana Margarida ;
Reeves, Kaajal ;
Martin, Cesar ;
Bourbon, Mafalda .
ATHEROSCLEROSIS, 2018, 277 :448-456
[6]   Novel functional APOB mutations outside LDL-binding region causing familial hypercholesterolaemia [J].
Alves, Ana Catarina ;
Etxebarria, Aitor ;
Soutar, Anne Katherine ;
Martin, Cesar ;
Bourbon, Mafalda .
HUMAN MOLECULAR GENETICS, 2014, 23 (07) :1817-1828
[7]  
[Anonymous], 1991, BMJ
[8]   Matrix metalloproteinase inhibition with tetracyclines for the treatment of coronary artery disease [J].
Bench, Travis J. ;
Jeremias, Allen ;
Brown, David L. .
PHARMACOLOGICAL RESEARCH, 2011, 64 (06) :561-566
[9]   Validation of LDLr Activity as a Tool to Improve Genetic Diagnosis of Familial Hypercholesterolemia: A Retrospective on Functional Characterization of LDLr Variants [J].
Benito-Vicente, Asier ;
Uribe, Kepa B. ;
Jebari, Shifa ;
Galicia-Garcia, Unai ;
Ostolaza, Helena ;
Martin, Cesar .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2018, 19 (06)
[10]   The importance of an integrated analysis of clinical, molecular, and functional data for the genetic diagnosis of familial hypercholesterolemia [J].
Benito-Vicente, Asier ;
Alves, Ana Catarina ;
Etxebarria, Aitor ;
Medeiros, Ana Medeiros ;
Martin, Cesar ;
Bourbon, Mafalda .
GENETICS IN MEDICINE, 2015, 17 (12) :980-988