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Novel Therapeutic Approaches for the Management of Elevated Lipoprotein(a): From Traditional Agents to Future Treatment Options.

作者信息

Paragh György, Zilahi Péter, Kolozsvári László Róbert, Lőrincz Hajnalka, Fülöp Péter, Harangi Mariann

机构信息

Division of Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.

Department of Family and Occupational Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.

出版信息

Life (Basel). 2024 Mar 12;14(3):374. doi: 10.3390/life14030374.


DOI:10.3390/life14030374
PMID:38541699
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10971318/
Abstract

Cardiovascular disease is the leading cause of mortality worldwide. Despite the availability of effective low-density lipoprotein cholesterol (LDL-C) lowering agents, an increased cardiovascular risk is still observed in individuals with therapeutic LDL-C levels. One of these cardiovascular risk factors is elevated plasma lipoprotein(a) (Lp(a)) concentration, which maintains chronic inflammation through the increased presence of oxidized phospholipids on its surface. In addition, due to its 90 percent homology with the fibrinolytic proenzyme plasminogen, Lp(a) exhibits atherothrombotic effects. These may also contribute to the increased cardiovascular risk in individuals with high Lp(a) levels that previous epidemiological studies have shown to exist independently of LDL-C and other lipid parameters. In this review, the authors overview the novel therapeutic options to achieve effective Lp(a) lowering treatment, which may help to define tailored personalized medicine and reduce the residual cardiovascular risk in high-risk patients. Agents that increase LDL receptor expression, including statins, proprotein convertase subtilisin kexin type 9 inhibitors, and LDL production inhibitors, are also discussed. Other treatment options, e.g., cholesterolester transfer protein inhibitors, nicotinic acid derivatives, thyroid hormone mimetics, lipoprotein apheresis, as well as apolipoprotein(a) reducing antisense oligonucleotides and small interfering RNAs, are also evaluated.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/38397ba5e259/life-14-00374-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/8b4d0143d741/life-14-00374-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/d0dfb9cd9a87/life-14-00374-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/38397ba5e259/life-14-00374-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/8b4d0143d741/life-14-00374-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/d0dfb9cd9a87/life-14-00374-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08bb/10971318/38397ba5e259/life-14-00374-g003.jpg

相似文献

[1]
Novel Therapeutic Approaches for the Management of Elevated Lipoprotein(a): From Traditional Agents to Future Treatment Options.

Life (Basel). 2024-3-12

[2]
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Int J Environ Res Public Health. 2023-9-6

[3]
From lipoprotein apheresis to proprotein convertase subtilisin/kexin type 9 inhibitors: Impact on low-density lipoprotein cholesterol and C-reactive protein levels in cardiovascular disease patients.

Eur J Prev Cardiol. 2018-7-30

[4]
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors: Present perspectives and future horizons.

Nutr Metab Cardiovasc Dis. 2016-10

[5]
Discordant response of low-density lipoprotein cholesterol and lipoprotein(a) levels to monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9.

J Clin Lipidol. 2017

[6]
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J Am Coll Cardiol. 2013-8-21

[7]
Modern Approaches to Lower Lipoprotein(a) Concentrations and Consequences for Cardiovascular Diseases.

Biomedicines. 2021-9-20

[8]
Lipoprotein(a) and its Significance in Cardiovascular Disease: A Review.

JAMA Cardiol. 2022-7-1

[9]
Proprotein convertase subtilisin/kexin 9 inhibitors: an emerging lipid-lowering therapy?

J Cardiovasc Pharmacol Ther. 2015-3

[10]
Lipoprotein(a) Lowering-From Lipoprotein Apheresis to Antisense Oligonucleotide Approach.

J Clin Med. 2020-7-3

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[1]
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Front Cardiovasc Med. 2025-7-1

[2]
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[3]
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本文引用的文献

[1]
Targeting Lipoprotein(a): Can RNA Therapeutics Provide the Next Step in the Prevention of Cardiovascular Disease?

Cardiol Ther. 2024-3

[2]
Novel Therapies for Lipoprotein(a): Update in Cardiovascular Risk Estimation and Treatment.

Curr Atheroscler Rep. 2024-4

[3]
Muvalaplin, an Oral Small Molecule Inhibitor of Lipoprotein(a) Formation: A Randomized Clinical Trial.

JAMA. 2023-9-19

[4]
Clinical applications of the CRISPR/Cas9 genome-editing system: Delivery options and challenges in precision medicine.

Genes Dis. 2023-3-25

[5]
Clinical Trial Design for Lipoprotein(a)-Lowering Therapies: JACC Focus Seminar 2/3.

J Am Coll Cardiol. 2023-4-25

[6]
Potential Novel RNA-Targeting Agents for Effective Lipoprotein(a) Lowering: A Systematic Assessment of the Evidence From Completed and Ongoing Developmental Clinical Trials.

J Cardiovasc Pharmacol. 2023-7-1

[7]
Small Interfering RNA to Reduce Lipoprotein(a) in Cardiovascular Disease.

N Engl J Med. 2022-11-17

[8]
Efficacy and Safety of an Investigational Single-Course CRISPR Base-Editing Therapy Targeting in Nonhuman Primate and Mouse Models.

Circulation. 2023-1-17

[9]
Consensus and guidelines on lipoprotein(a) - seeing the forest through the trees.

Curr Opin Lipidol. 2022-12-1

[10]
Cholesteryl Ester Transfer Protein Inhibition Reduces Major Adverse Cardiovascular Events by Lowering Apolipoprotein B Levels.

Int J Mol Sci. 2022-8-20

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