LP(a): Structure, Genetics, Associated Cardiovascular Risk, and Emerging Therapeutics

Lipoprotein(a) [Lp(a)] is a molecule bound to apolipoprotein(a) with some similarity to low-density lipoprotein cholesterol (LDL-C), which has been found to be a risk factor for cardiovascular disease (CVD). Lp(a) appears to induce inflammation, atherogenesis, and thrombosis. Approximately 20% of th...

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Vydáno v:Annual review of pharmacology and toxicology Ročník 64; s. 135
Hlavní autoři: Tasdighi, Erfan, Adhikari, Rishav, Almaadawy, Omar, Leucker, Thorsten M, Blaha, Michael J
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 23.01.2024
Témata:
Cardiovascular Diseases - drug therapy
Cardiovascular Diseases - genetics
Cholesterol, LDL - metabolism
Cholesterol, LDL - therapeutic use
Heart Disease Risk Factors
Humans
Lipoprotein(a) - genetics
Lipoprotein(a) - metabolism
Lipoprotein(a) - therapeutic use
Risk Factors
atherosclerosis
clinical trial
cardiovascular disease
lipoprotein(a)
therapy
antisense oligonucleotides
ISSN:1545-4304, 1545-4304
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Popis
Shrnutí:Lipoprotein(a) [Lp(a)] is a molecule bound to apolipoprotein(a) with some similarity to low-density lipoprotein cholesterol (LDL-C), which has been found to be a risk factor for cardiovascular disease (CVD). Lp(a) appears to induce inflammation, atherogenesis, and thrombosis. Approximately 20% of the world's population has increased Lp(a) levels, determined predominantly by genetics. Current clinical practices for the management of dyslipidemia are ineffective in lowering Lp(a) levels. Evolving RNA-based therapeutics, such as the antisense oligonucleotide pelacarsen and small interfering RNA olpasiran, have shown promising results in reducing Lp(a) levels. Phase III pivotal cardiovascular outcome trials [Lp(a)HORIZON and OCEAN(a)] are ongoing to evaluate their efficacy in secondary prevention of major cardiovascular events in patients with elevated Lp(a). The future of cardiovascular residual risk reduction may transition to a personalized approach where further lowering of either LDL-C, triglycerides, or Lp(a) is selected after high-intensity statin therapy based on the individual risk profile and preferences of each patient.
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ISSN:1545-4304
1545-4304
DOI:10.1146/annurev-pharmtox-031023-100609