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Review
. 2024 Feb 26;16(5):653.
doi: 10.3390/nu16050653.

High-Density Lipoprotein Metabolism and Function in Cardiovascular Diseases: What about Aging and Diet Effects?

Mojgan Morvaridzadeh  1 , Nada Zoubdane  1 , Javad Heshmati  1 , Mehdi Alami  1 , Hicham Berrougui  1 , Abdelouahed Khalil  1
Affiliations
Review

High-Density Lipoprotein Metabolism and Function in Cardiovascular Diseases: What about Aging and Diet Effects?

Mojgan Morvaridzadeh et al. Nutrients. .

Abstract

Cardiovascular diseases (CVDs) have become the leading global cause of mortality, prompting a heightened focus on identifying precise indicators for their assessment and treatment. In this perspective, the plasma levels of HDL have emerged as a pivotal focus, given the demonstrable correlation between plasma levels and cardiovascular events, rendering them a noteworthy biomarker. However, it is crucial to acknowledge that HDLs, while intricate, are not presently a direct therapeutic target, necessitating a more nuanced understanding of their dynamic remodeling throughout their life cycle. HDLs exhibit several anti-atherosclerotic properties that define their functionality. This functionality of HDLs, which is independent of their concentration, may be impaired in certain risk factors for CVD. Moreover, because HDLs are dynamic parameters, in which HDL particles present different atheroprotective properties, it remains difficult to interpret the association between HDL level and CVD risk. Besides the antioxidant and anti-inflammatory activities of HDLs, their capacity to mediate cholesterol efflux, a key metric of HDL functionality, represents the main anti-atherosclerotic property of HDL. In this review, we will discuss the HDL components and HDL structure that may affect their functionality and we will review the mechanism by which HDL mediates cholesterol efflux. We will give a brief examination of the effects of aging and diet on HDL structure and function.

Keywords: CVD; HDL; aging; diet; inflammation; lipoproteins; oxidative stress.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The main structure of a spherical HDL. LCAT: Lecithin–Cholesterol Acyltransferase, PLTP: Phospholipid Transfer Protein, PON1: Paraoxonase 1.
Figure 2
Figure 2
HDL maturation and RCT. ABCA1: ATP-binding cassette sub-family A member 1, ABCG1: ATP-binding cassette sub-family G member 1, Apo A-I: Apolipoprotein A-I, CETP: Cholesterol Ester Transfer Protein, CLA-1: CD36 and LIMPII analogous-1, E-Ch: Esterified Cholesterol, F-Ch: Free Cholesterol, HDL: High-Density Lipoprotein, LCAT: Lecithin–Cholesterol Acyltransferase, LDL: Low-Density Lipoprotein, P: Phospholipid, PLTP: Phospholipid Transfer Protein, SM: Sphingomyelin, SR-B-I: Scavenger Receptor class B type I, TG: Triglycerides, VLDL: Very-Low-Density Lipoprotein.
Figure 3
Figure 3
The interrelationships between aging, HDL, and CVD. ABCA1: ATP-binding cassette sub-family A member 1, ABCG1: ATP-binding cassette sub-family G member 1, Apo: Apolipoprotein, F-Ch: Free Cholesterol, HDL: High-Density Lipoprotein, MPO: Myeloperoxidase, PLTP: Phospholipid Transfer Protein, PON1: Paraoxonase 1, RCT: Reverse Cholesterol Transport, SAA: Serum Amyloid A, SM: Sphingomyelin, TG: Triglyceride.
See this image and copyright information in PMC

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