The Importance of Lipoprotein Lipase Regulation in Atherosclerosis.

ANGPTL atherosclerosis lipoprotein lipase

Journal

Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304

Informations de publication

Date de publication:
06 Jul 2021
Historique:
received: 31 05 2021
revised: 02 07 2021
accepted: 04 07 2021
entrez: 6 8 2021
pubmed: 7 8 2021
medline: 7 8 2021
Statut: epublish

Résumé

Lipoprotein lipase (LPL) plays a major role in the lipid homeostasis mainly by mediating the intravascular lipolysis of triglyceride rich lipoproteins. Impaired LPL activity leads to the accumulation of chylomicrons and very low-density lipoproteins (VLDL) in plasma, resulting in hypertriglyceridemia. While low-density lipoprotein cholesterol (LDL-C) is recognized as a primary risk factor for atherosclerosis, hypertriglyceridemia has been shown to be an independent risk factor for cardiovascular disease (CVD) and a residual risk factor in atherosclerosis development. In this review, we focus on the lipolysis machinery and discuss the potential role of triglycerides, remnant particles, and lipolysis mediators in the onset and progression of atherosclerotic cardiovascular disease (ASCVD). This review details a number of important factors involved in the maturation and transportation of LPL to the capillaries, where the triglycerides are hydrolyzed, generating remnant lipoproteins. Moreover, LPL and other factors involved in intravascular lipolysis are also reported to impact the clearance of remnant lipoproteins from plasma and promote lipoprotein retention in capillaries. Apolipoproteins (Apo) and angiopoietin-like proteins (ANGPTLs) play a crucial role in regulating LPL activity and recent insights into LPL regulation may elucidate new pharmacological means to address the challenge of hypertriglyceridemia in atherosclerosis development.

Identifiants

pubmed: 34356847
pii: biomedicines9070782
doi: 10.3390/biomedicines9070782
pmc: PMC8301479
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Subventions

Organisme : Lundbeckfonden
ID : R230-2016-2930
Organisme : Novo Nordisk Fonden
ID : NNF17OC0026868
Organisme : Novo Nordisk Fonden
ID : NNF18OC0033864
Organisme : Novo Nordisk Fonden
ID : NNF20OC0063444
Organisme : Leducq Foundation
ID : 12CVD04
Organisme : Horizon 2020
ID : 801481
Organisme : Region Hovedstaden
ID : A6867

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Auteurs

Anni Kumari (A)

Finsen Laboratory, Rigshospitalet, DK-2200 Copenhagen N, Denmark.
Biotech Research and Innovation Centre (BRIC), University of Copenhagen, DK-2200 Copenhagen N, Denmark.

Kristian K Kristensen (KK)

Finsen Laboratory, Rigshospitalet, DK-2200 Copenhagen N, Denmark.
Biotech Research and Innovation Centre (BRIC), University of Copenhagen, DK-2200 Copenhagen N, Denmark.

Michael Ploug (M)

Finsen Laboratory, Rigshospitalet, DK-2200 Copenhagen N, Denmark.
Biotech Research and Innovation Centre (BRIC), University of Copenhagen, DK-2200 Copenhagen N, Denmark.

Anne-Marie Lund Winther (AL)

Finsen Laboratory, Rigshospitalet, DK-2200 Copenhagen N, Denmark.
Biotech Research and Innovation Centre (BRIC), University of Copenhagen, DK-2200 Copenhagen N, Denmark.

Classifications MeSH