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Editorial
. 2019 Nov 26;11(11):256-265.
doi: 10.4330/wjc.v11.i11.256.

Novel lipid-modifying therapies addressing unmet needs in cardiovascular disease

Affiliations
Editorial

Novel lipid-modifying therapies addressing unmet needs in cardiovascular disease

Constantine E Kosmas et al. World J Cardiol. .

Abstract

Cardiovascular disease (CVD) remains a major cause of morbidity and mortality worldwide. Currently, it is well established that dyslipidemia is one of the major risk factors leading to the development of atherosclerosis and CVD. Statins remain the standard-of-care in the treatment of hypercholesterolemia and their use has significantly reduced cardiovascular morbidity and mortality. In addition, recent advances in lipid-modifying therapies, such as the development of proprotein convertase subtilisin/kexin type 9 inhibitors, have further improved cardiovascular outcomes in patients with hypercholesterolemia. However, despite significant progress in the treatment of dyslipidemia, there is still considerable residual risk of recurring cardiovascular events. Furthermore, in some cases, an effective therapy for the identified primary cause of a specific dyslipidemia has not been found up to date. Thus, a number of novel pharmacological interventions are under early human trials, targeting different molecular pathways of lipid formation, regulation and metabolism. This editorial aims to discuss the current clinical and scientific data on new promising lipid-modifying therapies addressing unmet needs in CVD, which may prove beneficial in the near future.

Keywords: Cardiovascular disease; Dyslipidemia; Lipid-modifying therapies.

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Conflict of interest statement

Conflict-of-interest statement: Kosmas CE and Guzman E are members of the Dyslipidemia Speaker Bureau of Amgen, Inc. The other authors declare no potential conflict of interest.

Figures

Figure 1
Figure 1
Molecular pathways of action and effects of novel lipid-modifying therapies addressing unmet needs in cardiovascular disease. siRNA: Small interfering RNA; ACL: Adenosine triphosphate-citrate lyase; AMPK: Adenosine monophosphate-activated protein kinase; PPARs: Peroxisome proliferator-activated receptors; Apo: Apolipoprotein; ASO: Antisense oligonucleotide; PCSK9: Proprotein convertase subtilisin/kexin type 9; HMG-CoA: 3-hydroxy-3-methylglutaryl-CoA; Lp(a): Lipoprotein (a); LXRs: Liver X receptors; LDL-C: Low-density lipoprotein cholesterol; CEC: Cholesterol efflux capacity.

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