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APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism

PURPOSE OF REVIEW: Apolipoprotein C-III (ApoC-III) is a widely known player in triglyceride metabolism, and it has been recently recognized as a polyhedric factor which may regulate several pathways beyond lipid metabolism by influencing cardiovascular, metabolic, and neurological disease risk. This...

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Autores principales: Giammanco, Antonina, Spina, Rossella, Cefalù, Angelo B., Averna, Maurizio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9947064/
https://www.ncbi.nlm.nih.gov/pubmed/36689070
http://dx.doi.org/10.1007/s11883-023-01080-8
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author Giammanco, Antonina
Spina, Rossella
Cefalù, Angelo B.
Averna, Maurizio
author_facet Giammanco, Antonina
Spina, Rossella
Cefalù, Angelo B.
Averna, Maurizio
author_sort Giammanco, Antonina
collection PubMed
description PURPOSE OF REVIEW: Apolipoprotein C-III (ApoC-III) is a widely known player in triglyceride metabolism, and it has been recently recognized as a polyhedric factor which may regulate several pathways beyond lipid metabolism by influencing cardiovascular, metabolic, and neurological disease risk. This review summarizes the different functions of ApoC-III and underlines the recent findings related to its multifaceted pathophysiological role. RECENT FINDINGS: The role of ApoC-III has been implicated in HDL metabolism and in the development of atherosclerosis, inflammation, and ER stress in endothelial cells. ApoC-III has been recently considered an important player in insulin resistance mechanisms, lipodystrophy, diabetic dyslipidemia, and postprandial hypertriglyceridemia (PPT). The emerging evidence of the involvement of ApoC-III in the in the pathogenesis of Alzheimer’s disease open the way to further study if modification of ApoC-III level slows disease progression. Furthermore, ApoC-III is clearly linked to cardiovascular disease (CVD) risk, and progression of coronary artery disease (CAD) as well as the calcification of aortic valve and recent clinical trials has pointed out the inhibition of ApoC-III as a promising approach to manage hypertriglyceridemia and prevent CVD. SUMMARY: Several evidences highlight the role of ApoC-III not only in triglyceride metabolism but also in several cardio-metabolic pathways. Results from recent clinical trials underline that the inhibition of ApoC-III is a promising therapeutical strategy for the management of severe hypertriglyceridemia and in CVD prevention.
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spelling pubmed-99470642023-02-24 APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism Giammanco, Antonina Spina, Rossella Cefalù, Angelo B. Averna, Maurizio Curr Atheroscler Rep Article PURPOSE OF REVIEW: Apolipoprotein C-III (ApoC-III) is a widely known player in triglyceride metabolism, and it has been recently recognized as a polyhedric factor which may regulate several pathways beyond lipid metabolism by influencing cardiovascular, metabolic, and neurological disease risk. This review summarizes the different functions of ApoC-III and underlines the recent findings related to its multifaceted pathophysiological role. RECENT FINDINGS: The role of ApoC-III has been implicated in HDL metabolism and in the development of atherosclerosis, inflammation, and ER stress in endothelial cells. ApoC-III has been recently considered an important player in insulin resistance mechanisms, lipodystrophy, diabetic dyslipidemia, and postprandial hypertriglyceridemia (PPT). The emerging evidence of the involvement of ApoC-III in the in the pathogenesis of Alzheimer’s disease open the way to further study if modification of ApoC-III level slows disease progression. Furthermore, ApoC-III is clearly linked to cardiovascular disease (CVD) risk, and progression of coronary artery disease (CAD) as well as the calcification of aortic valve and recent clinical trials has pointed out the inhibition of ApoC-III as a promising approach to manage hypertriglyceridemia and prevent CVD. SUMMARY: Several evidences highlight the role of ApoC-III not only in triglyceride metabolism but also in several cardio-metabolic pathways. Results from recent clinical trials underline that the inhibition of ApoC-III is a promising therapeutical strategy for the management of severe hypertriglyceridemia and in CVD prevention. Springer US 2023-01-23 2023 /pmc/articles/PMC9947064/ /pubmed/36689070 http://dx.doi.org/10.1007/s11883-023-01080-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Giammanco, Antonina
Spina, Rossella
Cefalù, Angelo B.
Averna, Maurizio
APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism
title APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism
title_full APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism
title_fullStr APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism
title_full_unstemmed APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism
title_short APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism
title_sort apoc-iii: a gatekeeper in controlling triglyceride metabolism
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9947064/
https://www.ncbi.nlm.nih.gov/pubmed/36689070
http://dx.doi.org/10.1007/s11883-023-01080-8
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