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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

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 36602

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,

Epidemiological, 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 HDL cardioprotective functions, 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.

This Special Issue is jointly organized between IJMS and Biomedicines journals. According to the Aims and Scope of these journals, articles showing basic studies in biochemistry, molecular biology, and molecular medicine can be submitted to IJMS, while articles presenting more clinical content can be submitted to Biomedicines.

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

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Published Papers (11 papers)

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Editorial

Jump to: Research, Review

4 pages, 211 KiB  
Editorial
High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad and the Future
by Josep Julve and Joan Carles Escolà-Gil
Biomedicines 2021, 9(8), 857; https://doi.org/10.3390/biomedicines9080857 - 22 Jul 2021
Cited by 2 | Viewed by 1444
Abstract
Epidemiological studies have shown that low levels of plasma high-density lipoprotein cholesterol (HDL-C) are associated with increased atherosclerotic cardiovascular disease (CVD) [...] Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)

Research

Jump to: Editorial, Review

14 pages, 489 KiB  
Article
Comparison of Plasma Lipoprotein Composition and Function in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
by Anna Bonaterra-Pastra, Sofia Fernández-de-Retana, Andrea Rivas-Urbina, Núria Puig, Sònia Benítez, Olalla Pancorbo, David Rodríguez-Luna, Francesc Pujadas, Maria del Mar Freijo, Silvia Tur, Maite Martínez-Zabaleta, Pere Cardona Portela, Rocío Vera, Lucia Lebrato-Hernández, Juan F. Arenillas, Soledad Pérez-Sánchez, Joan Montaner, Jose Luis Sánchez-Quesada and Mar Hernández-Guillamon
Biomedicines 2021, 9(1), 72; https://doi.org/10.3390/biomedicines9010072 - 12 Jan 2021
Cited by 8 | Viewed by 2950
Abstract
Cerebral amyloid angiopathy (CAA) refers to beta-amyloid (Aβ) deposition in brain vessels and is clinically the main cause of lobar intracerebral hemorrhage (ICH). Aβ can also accumulate in brain parenchyma forming neuritic plaques in Alzheimer’s disease (AD). Our study aimed to determine whether [...] Read more.
Cerebral amyloid angiopathy (CAA) refers to beta-amyloid (Aβ) deposition in brain vessels and is clinically the main cause of lobar intracerebral hemorrhage (ICH). Aβ can also accumulate in brain parenchyma forming neuritic plaques in Alzheimer’s disease (AD). Our study aimed to determine whether the peripheral lipid profile and lipoprotein composition are associated with cerebral beta-amyloidosis pathology and may reflect biological differences in AD and CAA. For this purpose, lipid and apolipoproteins levels were analyzed in plasma from 51 ICH-CAA patients (collected during the chronic phase of the disease), 60 AD patients, and 60 control subjects. Lipoproteins (VLDL, LDL, and HDL) were isolated and their composition and pro/antioxidant ability were determined. We observed that alterations in the lipid profile and lipoprotein composition were remarkable in the ICH-CAA group compared to control subjects, whereas the AD group presented no specific alterations compared with controls. ICH-CAA patients presented an atheroprotective profile, which consisted of lower total and LDL cholesterol levels. Plasma from chronic ICH-CAA patients also showed a redistribution of ApoC-III from HDL to VLDL and a higher ApoE/ApoC-III ratio in HDL. Whether these alterations reflect a protective response or have a causative effect on the pathology requires further investigation. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
14 pages, 1964 KiB  
Article
HDL-Mediated Cholesterol Efflux and Plasma Loading Capacities Are Altered in Subjects with Metabolically- but Not Genetically Driven Non-Alcoholic Fatty Liver Disease (NAFLD)
by Alessia Di Costanzo, Annalisa Ronca, Laura D’Erasmo, Matteo Manfredini, Francesco Baratta, Daniele Pastori, Michele Di Martino, Fabrizio Ceci, Francesco Angelico, Maria Del Ben, Chiara Pavanello, Marta Turri, Laura Calabresi, Elda Favari and Marcello Arca
Biomedicines 2020, 8(12), 625; https://doi.org/10.3390/biomedicines8120625 - 18 Dec 2020
Cited by 20 | Viewed by 3134
Abstract
Background. Non-alcoholic fatty liver disease (NAFLD) increases the risk of atherosclerosis but this risk may differ between metabolically- vs. genetically-driven NAFLD. High-density lipoprotein (HDL)-mediated cholesterol efflux (CEC) and plasma loading capacity (CLC) are key factors in atherogenesis. Aims. To test whether [...] Read more.
Background. Non-alcoholic fatty liver disease (NAFLD) increases the risk of atherosclerosis but this risk may differ between metabolically- vs. genetically-driven NAFLD. High-density lipoprotein (HDL)-mediated cholesterol efflux (CEC) and plasma loading capacity (CLC) are key factors in atherogenesis. Aims. To test whether CEC and CLC differ between metabolically- vs. genetically-determined NAFLD. Methods: CEC and CLC were measured in 19 patients with metabolic NAFLD and wild-type PNPLA3 genotype (Group M), 10 patients with genetic NAFLD carrying M148M PNPLA3 genotype (Group G), and 10 controls PNPLA3 wild-types and without NAFLD. CEC and CLC were measured ex vivo by isotopic and fluorimetric techniques using cellular models. Results: Compared with Group G, Group M showed reduced total CEC (−18.6%; p < 0.001) as well as that mediated by cholesterol transporters (−25.3% ABCA1; −16.3% ABCG1; −14.8% aqueous diffusion; all p < 0.04). No difference in CEC was found between Group G and controls. The presence of metabolic syndrome further impaired ABCG1-mediated CEC in Group M. Group M had higher plasma-induced CLC than Group G and controls (p < 0.001). Conclusions: Metabolically-, but not genetically-, driven NAFLD associates with dysfunctional HDL-meditated CEC and abnormal CLC. These data suggest that the mechanisms of anti-atherogenic protection in metabolic NAFLD are impaired. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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16 pages, 3570 KiB  
Article
An Increased Plasma Level of ApoCIII-Rich Electronegative High-Density Lipoprotein May Contribute to Cognitive Impairment in Alzheimer’s Disease
by Hua-Chen Chan, Liang-Yin Ke, Hsiao-Ting Lu, Shih-Feng Weng, Hsiu-Chuan Chan, Shi-Hui Law, I-Ling Lin, Chuan-Fa Chang, Ye-Hsu Lu, Chu-Huang Chen and Chih-Sheng Chu
Biomedicines 2020, 8(12), 542; https://doi.org/10.3390/biomedicines8120542 - 26 Nov 2020
Cited by 6 | Viewed by 2156
Abstract
High-density lipoprotein (HDL) plays a vital role in lipid metabolism and anti-inflammatory activities; a dysfunctional HDL impairs cholesterol efflux pathways. To understand HDL’s role in patients with Alzheimer’s disease (AD), we analyzed the chemical properties and function. HDL from AD patients (AD-HDL) was [...] Read more.
High-density lipoprotein (HDL) plays a vital role in lipid metabolism and anti-inflammatory activities; a dysfunctional HDL impairs cholesterol efflux pathways. To understand HDL’s role in patients with Alzheimer’s disease (AD), we analyzed the chemical properties and function. HDL from AD patients (AD-HDL) was separated into five subfractions, H1–H5, using fast-protein liquid chromatography equipped with an anion-exchange column. Subfraction H5, defined as the most electronegative HDL, was increased 5.5-fold in AD-HDL (23.48 ± 17.83%) in comparison with the control HDL (4.24 ± 3.22%). By liquid chromatography mass spectrometry (LC/MSE), AD-HDL showed that the level of apolipoprotein (apo)CIII was elevated but sphingosine-1-phosphate (S1P)-associated apoM and anti-oxidative paraoxonase 1 (PON1) were reduced. AD-HDL showed a lower cholesterol efflux capacity that was associated with the post-translational oxidation of apoAI. Exposure of murine macrophage cell line, RAW 264.7, to AD-HDL induced a vibrant expression of ganglioside GM1 in colocalization with apoCIII on lipid rafts alongside a concomitant increase of tumor necrosis factor-α (TNF-α) detectable in the cultured medium. In conclusion, AD-HDL had a higher proportion of H5, an apoCIII-rich electronegative HDL subfraction. The associated increase in pro-inflammatory (apoCIII, TNF-α) components might favor Amyloid β assembly and neural inflammation. A compromised cholesterol efflux capacity of AD-HDL may also contribute to cognitive impairment. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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13 pages, 1629 KiB  
Article
Cholesterol Efflux Capacity and Cardiovascular Disease: The Ludwigshafen Risk and Cardiovascular Health (LURIC) Study
by Andreas Ritsch, Angela Duerr, Patrick Kahler, Monika Hunjadi, Tatjana Stojakovic, Guenther Silbernagel, Hubert Scharnagl, Marcus E. Kleber and Winfried März
Biomedicines 2020, 8(11), 524; https://doi.org/10.3390/biomedicines8110524 - 21 Nov 2020
Cited by 15 | Viewed by 2552
Abstract
(1) Background and Aims: Efforts to reduce coronary artery disease (CAD) by raising high-density lipoprotein (HDL) cholesterol (HDL-C) have not been uniformly successful. A more important factor than HDL-C may be cellular cholesterol efflux mediated by HDL, which has been shown to be [...] Read more.
(1) Background and Aims: Efforts to reduce coronary artery disease (CAD) by raising high-density lipoprotein (HDL) cholesterol (HDL-C) have not been uniformly successful. A more important factor than HDL-C may be cellular cholesterol efflux mediated by HDL, which has been shown to be associated with CAD. In this report, we analyzed the influence of cardiovascular biomarkers and risk factors on cholesterol efflux in a prospective observational study of patients referred to coronary angiography. (2) Methods: HDL-mediated efflux capacity was determined for 2468 participants of the Ludwigshafen Risk and Cardiovascular Health (LURIC) study who were referred to coronary angiography at baseline between 1997 and 2000. Median follow-up time was 9.9 years. Primary and secondary endpoints were cardiovascular and all-cause mortality, respectively. (3) Results: Cholesterol efflux strongly correlated with HDL-related markers including HDL cholesterol, HDL phospholipids, and apolipoproteins AI and AII, as well as HDL particle concentration, which was not seen for low density lipoprotein (LDL) markers including LDL cholesterol and apoB. Cholesterol efflux was associated negatively with C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), and serum amyloid A. Cardiovascular mortality was higher in patients in the lowest cholesterol efflux quartile. This association was weakened, but not fully abolished, after adjustment for HDL cholesterol. (4) Conclusions: We demonstrate that cholesterol efflux was associated with HDL-composition as well as inflammatory burden in patients referred for coronary angiography, and that this inversely predicts cardiovascular mortality independently of HDL cholesterol. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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14 pages, 1140 KiB  
Article
Phenol-Enriched Virgin Olive Oil Promotes Macrophage-Specific Reverse Cholesterol Transport In Vivo
by Lídia Cedó, Sara Fernández-Castillejo, Laura Rubió, Jari Metso, David Santos, Daniel Muñoz-Aguayo, Andrea Rivas-Urbina, Mireia Tondo, Karen Alejandra Méndez-Lara, Marta Farràs, Matti Jauhiainen, Maria-José Motilva, Montserrat Fitó, Francisco Blanco-Vaca, Rosa Solà and Joan Carles Escolà-Gil
Biomedicines 2020, 8(8), 266; https://doi.org/10.3390/biomedicines8080266 - 03 Aug 2020
Cited by 9 | Viewed by 3558
Abstract
The intake of olive oil (OO) enriched with phenolic compounds (PCs) promotes ex vivo HDL-mediated macrophage cholesterol efflux in humans. We aimed to determine the effects of PC-enriched virgin OO on reverse cholesterol transport (RevCT) from macrophages to feces in vivo. Female C57BL/6 [...] Read more.
The intake of olive oil (OO) enriched with phenolic compounds (PCs) promotes ex vivo HDL-mediated macrophage cholesterol efflux in humans. We aimed to determine the effects of PC-enriched virgin OO on reverse cholesterol transport (RevCT) from macrophages to feces in vivo. Female C57BL/6 mice were given intragastric doses of refined OO (ROO) and a functional unrefined virgin OO enriched with its own PC (FVOO) for 14 days. Our experiments included two independent groups of mice that received intragastric doses of the phenolic extract (PE) used to prepare the FVOO and the vehicle solution (saline), as control, for 14 days. FVOO intake led to a significant increase in serum HDL cholesterol and its ability to induce macrophage cholesterol efflux in vitro when compared with ROO group. This was concomitant with the enhanced macrophage-derived [3H]cholesterol transport to feces in vivo. PE intake per se also increased HDL cholesterol levels and significantly promoted in vivo macrophage-to-feces RevCT rate when compared with saline group. PE upregulated the expression of the main macrophage transporter involved in macrophage cholesterol efflux, the ATP binding cassettea1. Our data provide direct evidence of the crucial role of OO PCs in the induction of macrophage-specific RevCT in vivo. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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16 pages, 1425 KiB  
Article
Familial Combined Hyperlipidemia (FCH) Patients with High Triglyceride Levels Present with Worse Lipoprotein Function Than FCH Patients with Isolated Hypercholesterolemia
by Núria Puig, Inka Miñambres, Sonia Benítez, Pedro Gil, Margarida Grau-Agramunt, Andrea Rivas-Urbina, Antonio Pérez and José Luis Sánchez-Quesada
Biomedicines 2020, 8(1), 6; https://doi.org/10.3390/biomedicines8010006 - 06 Jan 2020
Cited by 6 | Viewed by 3678
Abstract
Lipoprotein characteristics were analyzed in familial combined hyperlipidemia (FCH) patients before and after statin treatment. Twenty-six FCH patients were classified according to the presence (HTG group, n = 13) or absence (normotriglyceridemic (NTG) group, n = 13) of hypertriglyceridemia. Fifteen healthy subjects comprised [...] Read more.
Lipoprotein characteristics were analyzed in familial combined hyperlipidemia (FCH) patients before and after statin treatment. Twenty-six FCH patients were classified according to the presence (HTG group, n = 13) or absence (normotriglyceridemic (NTG) group, n = 13) of hypertriglyceridemia. Fifteen healthy subjects comprised the control group. Lipid profile, inflammation markers, and qualitative characteristics of lipoproteins were assessed. Both groups of FCH subjects showed high levels of plasma C-reactive protein (CRP), lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and apolipoprotein J. Statins reverted the increased levels of Lp-PLA2 and CRP. Lipoprotein composition alterations detected in FCH subjects were much more frequent in the HTG group, leading to dysfunctional low-density lipoproteins (LDL) and high-density lipoproteins (HDL). In the HTG group, LDL was smaller, more susceptible to oxidation, and contained more electronegative LDL (LDL(-)) compared to the NTG and control groups. Regarding HDL, the HTG group had less Lp-PLA2 activity than the NTG and control groups. HDL from both FCH groups was less anti-inflammatory than HDL from the control group. Statins increased LDL size, decreased LDL(-), and lowered Lp-PLA2 in HDL from HTG. In summary, pro-atherogenic alterations were more frequent and severe in the HTG group. Statins improved some alterations, but many remained unchanged in HTG. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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7 pages, 339 KiB  
Article
Low High-Density Lipoprotein Cholesterol Predisposes to Coronary Artery Ectasia
by Jamal Jafari, Aner Daum, Jihad Abu Hamed, Azriel Osherov, Yan Orlov, Chaim Yosefy and Enrique Gallego-Colon
Biomedicines 2019, 7(4), 79; https://doi.org/10.3390/biomedicines7040079 - 07 Oct 2019
Cited by 7 | Viewed by 2781
Abstract
Coronary Artery Ectasia (CAE) is a phenomenon characterized by locally or diffuse coronary artery dilation of one or more coronary arteries. In the present study, the prevalence of acquired coronary ectasia and coronary risk factors for CAE was analyzed in patients undergoing cardiac [...] Read more.
Coronary Artery Ectasia (CAE) is a phenomenon characterized by locally or diffuse coronary artery dilation of one or more coronary arteries. In the present study, the prevalence of acquired coronary ectasia and coronary risk factors for CAE was analyzed in patients undergoing cardiac catheterization for suspected ischemic heart disease. We retrospectively analyzed 4000 patients undergoing coronary angiography for suspected coronary artery disease at our cardiac catheterization unit, and a total of 171 patients were selected. The study group was divided into three groups, 65 patients with CAE, 62 patients with significant obstructive coronary artery disease, and 44 patients with normal coronary angiograms as a control group. A negative correlation was observed between high-density lipoprotein cholesterol (HDL-C) and the presence of CAE (r = −0.274, p < 0.001). In addition, HDL-C (OR, 0.858; CI, 0.749–0.984; p = 0.029), low-density lipoprotein cholesterol (LDL-C)/HDL-C ratio (OR, 1.987; CI, 1.542–2.882; p = 0.034), and hemoglobin (OR, 2.060; CI, 1.114–3.809; p = 0.021) were identified as independent risk factors for the development of CAE. In fact, we observed that a one-unit increase in HDL-C corresponded to a 15% risk reduction in CAE development and that each unit increase in hemoglobin could potentially increase the CAE risk by 2-fold. Low HDL-C could significantly increase the risk of developing CAE in healthy individuals. Elevated hemoglobin could predispose to subsequent dilation and aneurysm of the coronary artery. This work suggests that disordered lipoprotein metabolism or altered hemoglobin values can predispose patients to aneurysmal coronary artery disease. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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15 pages, 4088 KiB  
Article
High Energy Intake Induced Overexpression of Transcription Factors and Its Regulatory Genes Involved in Acceleration of Hepatic Lipogenesis: A Rat Model for Type 2 Diabetes
by Suresh P. Khadke, Aniket A. Kuvalekar, Abhay M. Harsulkar and Nitin Mantri
Biomedicines 2019, 7(4), 76; https://doi.org/10.3390/biomedicines7040076 - 27 Sep 2019
Cited by 11 | Viewed by 3769
Abstract
Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by impaired insulin action and its secretion. The objectives of the present study were to establish an economical and efficient animal model, mimicking pathophysiology of human T2DM to understand probable molecular mechanisms in [...] Read more.
Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by impaired insulin action and its secretion. The objectives of the present study were to establish an economical and efficient animal model, mimicking pathophysiology of human T2DM to understand probable molecular mechanisms in context with lipid metabolism. In the present study, male Wistar rats were randomly divided into three groups. Animals were fed with high fat diet (HFD) except healthy control (HC) for 12 weeks. After eight weeks, intra peritoneal glucose tolerance test was performed. After confirmation of glucose intolerance, diabetic control (DC) group was injected with streptozotocin (STZ) (35 mg/kg b.w., i.p.). HFD fed rats showed increase (p ≤ 0.001) in glucose tolerance and HOMA-IR as compared to HC. Diabetes rats showed abnormal (p ≤ 0.001) lipid profile as compared to HC. The hepatocyte expression of transcription factors SREBP-1c and NFκβ, and their target genes were found to be upregulated, while PPAR-γ, CPT1A and FABP expressions were downregulated as compared to the HC. A number of animal models have been raised for studying T2DM, but the study has been restricted to only the biochemical level. The model is validated at biochemical, molecular and histopathological levels, which can be used for screening new therapeutics for the effective management of T2DM. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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Review

Jump to: Editorial, Research

25 pages, 1522 KiB  
Review
High-Density Lipoprotein (HDL) in Allergy and Skin Diseases: Focus on Immunomodulating Functions
by Athina Trakaki and Gunther Marsche
Biomedicines 2020, 8(12), 558; https://doi.org/10.3390/biomedicines8120558 - 01 Dec 2020
Cited by 19 | Viewed by 6079
Abstract
From an evolutionary perspective, lipoproteins are not only lipid transporters, but they also have important functions in many aspects of immunity. High-density lipoprotein (HDL) particles are the most abundant lipoproteins and the most heterogeneous in terms of their composition, structure, and biological functions. [...] Read more.
From an evolutionary perspective, lipoproteins are not only lipid transporters, but they also have important functions in many aspects of immunity. High-density lipoprotein (HDL) particles are the most abundant lipoproteins and the most heterogeneous in terms of their composition, structure, and biological functions. Despite strong evidence that HDL potently influences the activity of several immune cells, the role of HDL in allergies and skin diseases is poorly understood. Alterations in HDL-cholesterol levels have been observed in allergic asthma, allergic rhinitis, atopic dermatitis (eczema), psoriasis, urticaria, and angioedema. HDL-associated apolipoprotein (apo) A-I, apoA-IV, and apoC-III, and lyso-phosphatidylcholines potently suppress immune cell effector responses. Interestingly, recent studies provided evidence that allergies and skin diseases significantly affect HDL composition, metabolism, and function, which, in turn, could have a significant impact on disease progression, but may also affect the risk of cardiovascular disease and infections. Interestingly, not only a loss in function, but also, sometimes, a gain in function of certain HDL properties is observed. The objective of this review article is to summarize the newly identified changes in the metabolism, composition, and function of HDL in allergies and skin diseases. We aim to highlight the possible pathophysiological consequences with a focus on HDL-mediated immunomodulatory activities. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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20 pages, 2004 KiB  
Review
High-Density Lipoprotein Modifications: A Pathological Consequence or Cause of Disease Progression?
by Andrea Bonnin Márquez, Sumra Nazir and Emiel P.C. van der Vorst
Biomedicines 2020, 8(12), 549; https://doi.org/10.3390/biomedicines8120549 - 28 Nov 2020
Cited by 21 | Viewed by 3543
Abstract
High-density lipoprotein (HDL) is well-known for its cardioprotective effects, as it possesses anti-inflammatory, anti-oxidative, anti-thrombotic, and cytoprotective properties. Traditionally, studies and therapeutic approaches have focused on raising HDL cholesterol levels. Recently, it became evident that, not HDL cholesterol, but HDL composition and functionality, [...] Read more.
High-density lipoprotein (HDL) is well-known for its cardioprotective effects, as it possesses anti-inflammatory, anti-oxidative, anti-thrombotic, and cytoprotective properties. Traditionally, studies and therapeutic approaches have focused on raising HDL cholesterol levels. Recently, it became evident that, not HDL cholesterol, but HDL composition and functionality, is probably a more fruitful target. In disorders, such as chronic kidney disease or cardiovascular diseases, it has been observed that HDL is modified and becomes dysfunctional. There are different modification that can occur, such as serum amyloid, an enrichment and oxidation, carbamylation, and glycation of key proteins. Additionally, the composition of HDL can be affected by changes to enzymes such as cholesterol ester transfer protein (CETP), lecithin-cholesterol acyltransferase (LCAT), and phospholipid transfer protein (PLTP) or by modification to other important components. This review will highlight some main modifications to HDL and discuss whether these modifications are purely a consequential result of pathology or are actually involved in the pathology itself and have a causal role. Therefore, HDL composition may present a molecular target for the amelioration of certain diseases, but more information is needed to determine to what extent HDL modifications play a causal role in disease development. Full article
(This article belongs to the Special Issue High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad, and the Future)
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