| Autor: |
Tsioulos G; Fourth Department of Internal Medicine, Medical School, University General Hospital Attikon, National and Kapodistrian University of Athens, 12462 Athens, Greece., Kounatidis D; Second Department of Internal Medicine, School of Medicine, Hippokration General Hospital, National and Kapodistrian University of Athens, 11527 Athens, Greece., Vallianou NG; First Department of Internal Medicine, Sismanogleio General Hospital, 15126 Athens, Greece., Poulaki A; Hematology Unit, Second Department of Internal Medicine, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece., Kotsi E; Second Department of Internal Medicine, School of Medicine, Hippokration General Hospital, National and Kapodistrian University of Athens, 11527 Athens, Greece., Christodoulatos GS; Department of Microbiology, Sismanogleio General Hospital, 15126 Athens, Greece., Tsilingiris D; First Department of Internal Medicine, University Hospital of Alexandroupolis, Democritus University of Thrace, 68100 Alexandroupolis, Greece., Karampela I; Second Department of Critical Care, Attikon General University Hospital, Medical School, National and Kapodistrian University of Athens, 12462 Athens, Greece., Skourtis A; Department of Internal Medicine, Evangelismos General Hospital, 10676 Athens, Greece., Dalamaga M; Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece. |
| Abstrakt: |
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. |
