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Lipoproteins: From the Vital Role in Lipid Metabolism to Risk...
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Lipoproteins: From the Vital Role in Lipid Metabolism to Risk Factors for Atherosclerosis and Future Challenging Therapies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Lipids".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 6692

Special Issue Editors

Dr. Camelia Sorina Stancu

E-Mail Website
Guest Editor
Head of Lipoproteins and Atherosclerosis Laboratory, Lipidomics Department, Institute of Cellular Biology and Pathology “Nicolae Simionescu” of the Romanian Academy, Bucharest, Romania
Interests: Lipoproteins composition and their biosynthesis in the liver and small intestine; modified lipoproteins and their effects on the cells of the arterial wall; animal models and cell culture; anti-atherosclerotic therapies
Dr. Loredan Stefan Niculescu

E-Mail Website
Guest Editor
Head of Molecular Biology of Lipoproteins Laboratory, Lipidomics Department, Institute of Cellular Biology and Pathology “Nicolae Simionescu” of the Romanian Academy, Bucharest, Romania
Interests: Non-coding RNAs; microRNAs; RNA-related epigenetic alterations in dyslipidemia; atherosclerosis and diabetes; disease biomarkers; bioinformatics; in vivo modulation of microRNAs

Special Issue Information

Dear Colleagues,

It is well known that lipoproteins play a crucial role in the proper function of the cells as transporters of hydrophobic lipids through the aqueous body fluids for the needs of all tissues. Under certain pathologic conditions, the lipoproteins become risk factors for the development of atherosclerotic lesions in the arterial wall. A lot is known about the mechanisms by which modified lipoproteins induce and advance the atheroma formation. Their complex composition and the delicate balance between the beneficial and detrimental effects of their modified structure and components are under investigation and debate. The discovery that lipoproteins are carriers of non-coding RNAs has opened new research opportunities for these macromolecular complexes. The revolutionary statins therapy prolonged the life expectancy of cardiovascular disease (CVD) patients and improved their life quality, but residual risks of fatal events still remain. A challenge for the future CVD treatment is the development of new therapies to prevent or delay the atheroma formation and to considerably diminish the incidence of life-threatening events in patients at risk.

Dr. Camelia Sorina Stancu
Dr. Loredan Stefan Niculescu
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. Biomolecules 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 2700 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

  • Lipoproteins
  • Atherosclerosis
  • Apolipoproteins
  • Lipid metabolism
  • Arterial wall
  • Cell signaling
  • Epigenetics
  • Non-coding RNAs
  • Lipoproteins as biomarkers
  • Anti-atherosclerotic therapies

Published Papers (3 papers)

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Research

14 pages, 1977 KiB  
Article
CRISPR/dCas9 Transcriptional Activation of Endogenous Apolipoprotein AI and Paraoxonase 1 in Enterocytes Alleviates Endothelial Cell Dysfunction
by Laura Toma, Teodora Barbălată, Gabriela M. Sanda, Loredan S. Niculescu, Anca V. Sima and Camelia S. Stancu
Biomolecules 2021, 11(12), 1769; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11121769 - 25 Nov 2021
Cited by 2 | Viewed by 2083
Abstract
Atherosclerosis is the main cause of cardiovascular diseases with high prevalence worldwide. A promising therapeutic strategy to reverse atherosclerotic process is to improve the athero-protective potential of high-density lipoproteins (HDL). Since the small intestine is a source of HDL, we aimed to activate [...] Read more.
Atherosclerosis is the main cause of cardiovascular diseases with high prevalence worldwide. A promising therapeutic strategy to reverse atherosclerotic process is to improve the athero-protective potential of high-density lipoproteins (HDL). Since the small intestine is a source of HDL, we aimed to activate transcription of the endogenous HDL major proteins, apolipoprotein AI (ApoAI) and paraoxonase 1 (PON1), in enterocytes, and to evaluate their potential to correct the pro-inflammatory status of endothelial cells (EC). Caco-2 enterocytes were transfected with CRISPR activation plasmids targeting ApoAI or PON1, and their gene and protein expression were measured in cells and conditioned medium (CM). ATP binding cassette A1 and G8 transporters (ABCA1, ABCG8), scavenger receptor BI (SR-BI), and transcription regulators peroxisome proliferator-activated receptor γ (PPARγ), liver X receptors (LXRs), and sirtuin-1 (SIRT1) were assessed. Anti-inflammatory effects of CM from transfected enterocytes were estimated through its ability to inhibit tumor necrosis factor α (TNFα) activation of EC. Transcriptional activation of ApoAI or PON1 in enterocytes induces: (i) increase of their gene and protein expression, and secretion in CM; (ii) stimulation of ABCA1/G8 and SR-BI; (iii) upregulation of PPARγ, LXRs, and SIRT1. CM from transfected enterocytes attenuated the TNFα-induced inflammatory and oxidative stress in EC, by decreasing TNF receptor 1, monocyte chemoattractant protein-1, and p22phox. In conclusion, transcriptional activation of endogenous ApoAI or PON1 in enterocytes by CRISPR/dCas9 system is a realistic approach to stimulate biogenesis and function of major HDL proteins which can regulate cholesterol efflux transporters and reduce the inflammatory stress in activated EC. Full article
(This article belongs to the Special Issue Lipoproteins: From the Vital Role in Lipid Metabolism to Risk Factors for Atherosclerosis and Future Challenging Therapies)
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10 pages, 904 KiB  
Article
Immature Circulating SP-B, Bound to HDL, Represents an Early Sign of Smoke-Induced Pathophysiological Alterations
by Cristina Banfi, Maura Brioschi, Massimo Mapelli, Erica Gianazza, Alice Mallia, Beatrice Zoanni, Elisabetta Salvioni, Paola Gugliandolo, Nicolò Capra, Fabrizio Veglia and Piergiuseppe Agostoni
Biomolecules 2021, 11(4), 551; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11040551 - 09 Apr 2021
Cited by 3 | Viewed by 1842
Abstract
Cigarette smoking is a major independent risk factor for cardiovascular diseases (CVD). The underlying mechanisms, however, are not clearly understood. Lungs are the primary route of exposure to smoke, with pulmonary cells and surfactant being the first structures directly exposed, resulting in the [...] Read more.
Cigarette smoking is a major independent risk factor for cardiovascular diseases (CVD). The underlying mechanisms, however, are not clearly understood. Lungs are the primary route of exposure to smoke, with pulmonary cells and surfactant being the first structures directly exposed, resulting in the leakage of the immature proteoform of surfactant protein B (proSP-B). Herein, we evaluated whether proSP-B joined the cargo of high-density lipoprotein (HDL) proteins in healthy young subjects (n = 106) without any CVD risk factor other than smoking, and if HDL-associated proSP-B (HDL-SPB) correlated with pulmonary function parameters, systemic inflammation, and oxidative stress. At univariable analysis, HDL-SPB resulted significantly higher in smokers (2.2-fold, p < 0.001) than in non-smokers. No significant differences have been detected between smokers and non-smokers for inflammation, oxidation variables, and alveolar-capillary diffusion markers. In a multivariable model, HDL-SPB was independently associated with smoking. In conclusion, HDL-SPB is not only a precocious and sensitive index of the acute effects of smoke, but it might be also a potential causal factor in the onset of the vascular damage induced by modified HDL. These findings contribute to the emerging concept that the quality of the HDL proteome, rather than the quantity of particles, plays a central role in CVD risk protection. Full article
(This article belongs to the Special Issue Lipoproteins: From the Vital Role in Lipid Metabolism to Risk Factors for Atherosclerosis and Future Challenging Therapies)
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10 pages, 1868 KiB  
Article
Lipoprotein(a) and Cardiovascular Outcomes after Revascularization of Carotid and Lower Limbs Arteries
by Marat V. Ezhov, Narek A. Tmoyan, Olga I. Afanasieva, Marina I. Afanasieva and Sergei N. Pokrovsky
Biomolecules 2021, 11(2), 257; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11020257 - 10 Feb 2021
Cited by 6 | Viewed by 1981
Abstract
Background: Despite high-intensity lipid-lowering therapy, there is a residual risk of cardiovascular events that could be associated with lipoprotein(a) (Lp(a)). It has been shown that there is an association between elevated Lp(a) level and cardiovascular outcomes in patients with coronary heart disease. Data [...] Read more.
Background: Despite high-intensity lipid-lowering therapy, there is a residual risk of cardiovascular events that could be associated with lipoprotein(a) (Lp(a)). It has been shown that there is an association between elevated Lp(a) level and cardiovascular outcomes in patients with coronary heart disease. Data about the role of Lp(a) in the development of cardiovascular events after peripheral revascularization are scarce. Purpose: To evaluate the relationship of Lp(a) level with cardiovascular outcomes after revascularization of carotid and lower limbs arteries. Methods: The study included 258 patients (209 men, mean age 67 years) with severe carotid and/or lower extremity artery disease, who underwent successful elective peripheral revascularization. The primary endpoint was the composite of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. The secondary endpoint was the composite of primary endpoint and repeated revascularization. Results: For 36-month follow-up, 29 (11%) primary and 128 (50%) secondary endpoints were registered. There was a greater risk of primary (21 (8%) vs. 8 (3%); hazard ratio (HR), 3.0; 95% confidence interval (CI) 1.5–6.3; p < 0.01) and secondary endpoints (83 (32%) vs. 45 (17%), HR, 2.8; 95% CI 2.0–4.0; p < 0.01) in patients with elevated Lp(a) level (≥30 mg/dL) compared to patients with Lp(a) < 30 mg/dL. Multivariable-adjusted Cox regression analysis revealed that Lp(a) was independently associated with the incidence of cardiovascular outcomes. Conclusions: Patients with peripheral artery diseases have a high risk of cardiovascular events. Lp(a) level above 30 mg/dL is significantly and independently associated with cardiovascular events during 3-year follow-up after revascularization of carotid and lower limbs arteries. Full article
(This article belongs to the Special Issue Lipoproteins: From the Vital Role in Lipid Metabolism to Risk Factors for Atherosclerosis and Future Challenging Therapies)
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