Lipoprotein(a) and Atherosclerotic Cardiovascular Disease: Where Do We Stand?

被引：9

作者：

Tsioulos, Georgios ^{[1
]}

Kounatidis, Dimitris ^{[2
]}

Vallianou, Natalia G. ^{[3
]}

Poulaki, Aikaterini ^{[4
]}

Kotsi, Evangelia ^{[2
]}

Christodoulatos, Gerasimos Socrates ^{[5
]}

Tsilingiris, Dimitrios ^{[6
]}

Karampela, Irene ^{[7
]}

Skourtis, Alexandros ^{[8
]}

Dalamaga, Maria ^{[9
]}

机构：

[1] Natl & Kapodistrian Univ Athens, Univ Gen Hosp Attikon, Med Sch, Dept Internal Med 4, Athens 12462, Greece

[2] Natl & Kapodistrian Univ Athens, Hippokrat Gen Hosp, Sch Med, Dept Internal Med 2, Athens 11527, Greece

[3] Sismanogleio Gen Hosp, Dept Internal Med 1, Athens 15126, Greece

[4] Natl & Kapodistrian Univ Athens, Sch Med, Dept Internal Med 2, Hematol Unit, Athens 11527, Greece

[5] Sismanogleio Gen Hosp, Dept Microbiol, Athens 15126, Greece

[6] Democritus Univ Thrace, Univ Hosp Alexandroupolis, Dept Internal Med 1, Alexandroupolis 68100, Greece

[7] Natl & Kapodistrian Univ Athens, Attikon Gen Univ Hosp, Med Sch, Dept Crit Care 2, Athens 12462, Greece

[8] Evangelismos Gen Hosp, Dept Internal Med, Athens 10676, Greece

[9] Natl & Kapodistrian Univ Athens, Med Sch, Dept Biol Chem, Athens 11527, Greece

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2024年 / 25卷 / 06期

关键词：

antisense oligonucleotides; atherosclerosis; cardiovascular disease; chronic inflammation; lepodisiran; lipoprotein(a); muvalaplin; small interfering RNAs; TRANSFER PROTEIN-INHIBITION; GENOME-WIDE ASSOCIATION; APOLIPOPROTEIN(A) ISOFORM SIZE; EXTENDED-RELEASE NIACIN; C-REACTIVE PROTEIN; OXIDIZED PHOSPHOLIPIDS; ELEVATED LIPOPROTEIN(A); REDUCES LIPOPROTEIN(A); STATIN TREATMENT; LOW-DENSITY;

D O I：

10.3390/ijms25063537

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：

Lipoprotein(a) [Lp(a)] consists of a low-density lipoprotein-like molecule and an apolipoprotein(a) [apo(a)] particle. Lp(a) has been suggested to be an independent risk factor of atherosclerotic cardiovascular disease (ASCVD). Lp(a) plasma levels are considered to be 70-90% genetically determined through the codominant expression of the LPA gene. Therefore, Lp(a) levels are almost stable during an individual's lifetime. This lifelong stability, together with the difficulties in measuring Lp(a) levels in a standardized manner, may account for the scarcity of available drugs targeting Lp(a). In this review, we synopsize the latest data regarding the structure, metabolism, and factors affecting circulating levels of Lp(a), as well as the laboratory determination measurement of Lp(a), its role in the pathogenesis of ASCVD and thrombosis, and the potential use of various therapeutic agents targeting Lp(a). In particular, we discuss novel agents, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) that are currently being developed and target Lp(a). The promising role of muvalaplin, an oral inhibitor of Lp(a) formation, is then further analyzed.

引用

页数：35

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