ApoCIII: A multifaceted protein in cardiometabolic disease.

APOC3 gene APOC3 gene expression ApoCIII protein Cardiovascular disease risk Therapeutic target Triglycerides Triglycerides (TG)-rich lipoproteins (TRL)

Journal

Metabolism: clinical and experimental
ISSN: 1532-8600
Titre abrégé: Metabolism
Pays: United States
ID NLM: 0375267

Informations de publication

Date de publication:
12 2020
Historique:
received: 08 04 2020
revised: 20 09 2020
accepted: 26 09 2020
pubmed: 16 10 2020
medline: 22 12 2020
entrez: 15 10 2020
Statut: ppublish

Résumé

ApoCIII has a well-recognized role in triglyceride-rich lipoproteins metabolism. A considerable amount of data has clearly highlighted that high levels of ApoCIII lead to hypertriglyceridemia and, thereby, may influence the risk of cardiovascular disease. However, recent findings indicate that ApoCIII might also act beyond lipid metabolism. Indeed, ApoCIII has been implicated in other physiological processes such as glucose homeostasis, monocyte adhesion, activation of inflammatory pathways, and modulation of the coagulation cascade. As the inhibition of ApoCIII is emerging as a new promising therapeutic strategy, the complete understanding of multifaceted pathophysiological role of this apoprotein may be relevant. Therefore, the purpose of this work is to review available evidences not only related to genetics and biochemistry of ApoCIII, but also highlighting the role of this apoprotein in triglyceride and glucose metabolism, in the inflammatory process and coagulation cascade as well as in cardiovascular disease.

Identifiants

pubmed: 33058850
pii: S0026-0495(20)30259-6
doi: 10.1016/j.metabol.2020.154395
pii:
doi:

Substances chimiques

Apolipoprotein C-III 0
Blood Glucose 0
Triglycerides 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

154395

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest LD has received personal fees for public speaking, consultancy or grant support from Amryt Pharmaceuticals, Akcea Therapeutics, Pfizer, Amgen and Sanofi; MA has received research grant support from Amryth Pharmaceutical, Amgen, IONIS, Akcea Therapeutics, Pfizer and Sanofi; has served as a consultant for Amgen, Aegerion, Akcea Therapeutics, Regeneron, Sanofi and Alfasigma and received lecturing fees from Amgen, Amryth Pharmaceutical, Pfizer, Sanofi and AlfaSigma; AG has received personal fees for public speaking or consultancy support from Akcea Therapeutics, AMGEN, MSD, Mylan, Novartis, Sanofi and Regeneron, Unilever; EB has received honoraria from AMGEN, MSD, Sanofi and Regeneron, Unilever, Danone, Aegerion, Chiesi, Rottapharm-MEDA, Servier, Ionis-pharmaceuticals, AKCEA and MYLAN. ADC does not have any potential conflict of interest.

Auteurs

Laura D'Erasmo (L)

Department of Translational and Precision Medicine, Sapienza University of Rome, Italy; Department of Endocrinology and Cardiovascular Disease Prevention, Assistance Publique-Hôpitaux de Paris, La Pitié-Salpêtrière Hospital, Sorbonne University Paris, France. Electronic address: laura.derasmo@uniroma1.it.

Alessia Di Costanzo (A)

Department of Translational and Precision Medicine, Sapienza University of Rome, Italy. Electronic address: alessia.dicostanzo@uniroma1.it.

Antonio Gallo (A)

Department of Endocrinology and Cardiovascular Disease Prevention, Assistance Publique-Hôpitaux de Paris, La Pitié-Salpêtrière Hospital, Sorbonne University Paris, France.

Eric Bruckert (E)

Department of Endocrinology and Cardiovascular Disease Prevention, Assistance Publique-Hôpitaux de Paris, La Pitié-Salpêtrière Hospital, Sorbonne University Paris, France.

Marcello Arca (M)

Department of Translational and Precision Medicine, Sapienza University of Rome, Italy.

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Classifications MeSH