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Biomedicines
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High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and...
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High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future III

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 5878

Special Issue Editors

Dr. Joan Carles Escolà-Gil

E-Mail Website
Guest Editor
Institut d’Investigacions Biomèdiques (IIB) Sant Pau, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
Interests: atherosclerosis; cholesterol; genetically-modified mice; HDL; lipoproteins
Special Issues, Collections and Topics in MDPI journals
Dr. Josep Julve

E-Mail Website
Guest Editor
1. Institut de Recerca de l’Hospital de la Santa Creu i Sant Pau–Centre CERCA, Barcelona, Spain
2. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain
Interests: obesity; diabetes; lipoprotein metabolism; metabolic syndrome; therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Clinical and experimental studies have shown that low levels of plasma high-density lipoprotein (HDL) cholesterol are associated with increased atherosclerotic cardiovascular disease. Nevertheless, HDL-targeted drugs such as cholesteryl ester transfer protein inhibitors, fibrates, and niacin have failed to reduce cardiovascular events in clinical trials, thereby casting doubt on the beneficial effects of raising HDL levels.

Experimental studies have identified several cardioprotective functions of HDL, including the enhancement of macrophage reverse cholesterol transport and endothelial function, as well as its antioxidant, anti-inflammatory, and anti-thrombotic properties. HDL is highly heterogeneous and carries a large variety of lipids, proteins, and microRNAs. The different composition of HDL subpopulations is directly related to their cardioprotective functions, but the assignment of specific molecules to HDL functions is not completely understood.

Compelling available data strongly indicate that increased HDL cholesterol levels do not always correlate with enhanced beneficial HDL properties, thus questioning their potential as a biomarker of HDL functionality. In addition, the association between low HDL cholesterol and cardiovascular disease can be further confounded by several factors, including insulin resistance, inflammation, and/or metabolic derangements leading to altered plasma lipids, thereby indicating that low HDL levels could simply be a marker of an underlying pathology. Current research is moving towards both the development of robust HDL function tests and the identification of specific HDL molecules (many of them bioactive) within HDL that can be widely applied in translational and pre-clinical studies. The application of novel HDL-based approaches for therapeutic purposes requires the development of validated and reproducible measures of these key atheroprotective HDL functions.

Dr. Joan Carles Escolà-Gil
Dr. Josep Julve
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • atherosclerosis
  • cardiovascular
  • diabetes
  • cholesterol
  • HDL
  • inflammation
  • mice
  • oxidation
  • therapy

Related Special Issues

Published Papers (3 papers)

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Research

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16 pages, 4053 KiB  
Article
HDL-apoA-II Is Strongly Associated with 1-Year Mortality in Acute Heart Failure Patients
by Iva Klobučar, Vesna Degoricija, Ines Potočnjak, Matias Trbušić, Gudrun Pregartner, Andrea Berghold, Eva Fritz-Petrin, Hansjörg Habisch, Tobias Madl and Saša Frank
Biomedicines 2022, 10(7), 1668; https://doi.org/10.3390/biomedicines10071668 - 11 Jul 2022
Cited by 7 | Viewed by 1498
Abstract
The prognostic value of the subset of high-density lipoprotein (HDL) particles containing apolipoprotein (apo)A-II (HDL-apoA-II) in acute heart failure (AHF) remains unexplored. In this study, baseline serum levels of HDL-apoA-II (total and subfractions 1–4) were measured in 315 AHF patients using NMR spectroscopy. [...] Read more.
The prognostic value of the subset of high-density lipoprotein (HDL) particles containing apolipoprotein (apo)A-II (HDL-apoA-II) in acute heart failure (AHF) remains unexplored. In this study, baseline serum levels of HDL-apoA-II (total and subfractions 1–4) were measured in 315 AHF patients using NMR spectroscopy. The mean patient age was 74.2 ± 10.5 years, 136 (43.2%) were female, 288 (91.4%) had a history of cardiomyopathy, 298 (94.6%) presented as New York Heart Association class 4, and 118 (37.5%) patients died within 1 year after hospitalization for AHF. Multivariable Cox regression analyses, adjusted for age and sex as well as other clinical and laboratory parameters associated with 1-year mortality in the univariable analyses, revealed a significant inverse association of HDL-apoA-II (hazard ratio (HR) 0.67 per 1 standard deviation (1 SD) increase, 95% confidence interval (CI) 0.47–0.94, p = 0.020), HDL2-apoA-II (HR 0.72 per 1 SD increase, 95% CI 0.54–0.95, p = 0.019), and HDL3-apoA-II (HR 0.59 per 1 SD increase, 95% CI 0.43–0.80, p < 0.001) with 1-year mortality. We conclude that low baseline HDL-apoA-II, HDL2-apoA-II, and HDL3-apoA-II serum levels are associated with increased 1-year mortality in AHF patients and may thus be of prognostic value in AHF. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future III)
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16 pages, 2321 KiB  
Article
Thioredoxin Domain Containing 5 Suppression Elicits Serum Amyloid A-Containing High-Density Lipoproteins
by Javier Sánchez-Marco, Roberto Martínez-Beamonte, Alicia De Diego, Tania Herrero-Continente, Cristina Barranquero, Carmen Arnal, Joaquín Surra, María A. Navarro and Jesús Osada
Biomedicines 2022, 10(3), 709; https://doi.org/10.3390/biomedicines10030709 - 18 Mar 2022
Cited by 3 | Viewed by 1891
Abstract
Thioredoxin domain containing 5 (TXNDC5) is a protein disulfide isomerase involved in several diseases related to oxidative stress, energy metabolism and cellular inflammation. In a previous manuscript, a negative association between fatty liver development and hepatic Txndc5 expression was observed. To study the [...] Read more.
Thioredoxin domain containing 5 (TXNDC5) is a protein disulfide isomerase involved in several diseases related to oxidative stress, energy metabolism and cellular inflammation. In a previous manuscript, a negative association between fatty liver development and hepatic Txndc5 expression was observed. To study the role of TXNDC5 in the liver, we generated Txndc5-deficient mice. The absence of the protein caused an increased metabolic need to gain weight along with a bigger and fatter liver. RNAseq was performed to elucidate the putative mechanisms, showing a substantial liver overexpression of serum amyloid genes (Saa1, Saa2) with no changes in hepatic protein, but discrete plasma augmentation by the gene inactivation. Higher levels of malonyldialdehyde, apolipoprotein A1 and platelet activating factor-aryl esterase activity were also found in serum from Txndc5-deficient mice. However, no difference in the distribution of high-density lipoproteins (HDL)-mayor components and SAA was found between groups, and even the reactive oxygen species decreased in HDL coming from Txndc5-deficient mice. These results confirm the relation of this gene with hepatic steatosis and with a fasting metabolic derive remedying an acute phase response. Likewise, they pose a new role in modulating the nature of HDL particles, and SAA-containing HDL particles are not particularly oxidized. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future III)
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Review

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16 pages, 1130 KiB  
Review
HDL as Bidirectional Lipid Vectors: Time for New Paradigms
by María Luna-Luna, Eric Niesor and Óscar Pérez-Méndez
Biomedicines 2022, 10(5), 1180; https://doi.org/10.3390/biomedicines10051180 - 20 May 2022
Cited by 5 | Viewed by 1952
Abstract
The anti-atherogenic properties of high-density lipoproteins (HDL) have been explained mainly by reverse cholesterol transport (RCT) from peripheral tissues to the liver. The RCT seems to agree with most of the negative epidemiological correlations between HDL cholesterol levels and coronary artery disease. However, [...] Read more.
The anti-atherogenic properties of high-density lipoproteins (HDL) have been explained mainly by reverse cholesterol transport (RCT) from peripheral tissues to the liver. The RCT seems to agree with most of the negative epidemiological correlations between HDL cholesterol levels and coronary artery disease. However, therapies designed to increase HDL cholesterol failed to reduce cardiovascular risk, despite their capacity to improve cholesterol efflux, the first stage of RCT. Therefore, the cardioprotective role of HDL may not be explained by RCT, and it is time for new paradigms about the physiological function of these lipoproteins. It should be considered that the main HDL apolipoprotein, apo AI, has been highly conserved throughout evolution. Consequently, these lipoproteins play an essential physiological role beyond their capacity to protect against atherosclerosis. We propose HDL as bidirectional lipid vectors carrying lipids from and to tissues according to their local context. Lipid influx mediated by HDL appears to be particularly important for tissue repair right on site where the damage occurs, including arteries during the first stages of atherosclerosis. In contrast, the HDL-lipid efflux is relevant for secretory cells where the fusion of intracellular vesicles drastically enlarges the cytoplasmic membrane with the potential consequence of impairment of cell function. In such circumstances, HDL could deliver some functional lipids and pick up not only cholesterol but an integral part of the membrane in excess, restoring the viability of the secretory cells. This hypothesis is congruent with the beneficial effects of HDL against atherosclerosis as well as with their capacity to induce insulin secretion and merits experimental exploration. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future III)
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