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High-Density Lipoprotein in Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 6027

Special Issue Editor


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Guest Editor
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1736, USA
Interests: atherosclerosis; lipid metabolism; HDL

Special Issue Information

Dear Colleagues,

The fatty streak develops as a response to specific lipids that are carried into the artery wall with LDL and that subsequently become oxidized as a result of exposure to the oxidative waste of the artery wall cells (the Yang). The opposing (calming) forces (the Yin) include the antioxidants present both within the LDL and within the microenvironments where the LDL is trapped. These antioxidants function to prevent the formation of the oxidized lipids. Other opposing (calming) forces include specific enzymes contained within LDL or associated with HDL that inactivate these biologically active lipids. The balance between the Yin and the Yang determines the response of the artery wall.

The effect of life style on lipoprotein metabolism, systemic inflammation and cardiovascular well being is well known. Nutritional habits, physical activity, normal sleep and optimal physical and mental pressure play major role in achieving a healthy and smart life style.

The anti oxidant, anti inflammatory HDL in the basal state contains enzymes that can destroy oxidized lipids that mediate a chronic inflammatory response. In this sense, HDL in the basal state is anti-inflammatory. Our group has shown that the alterations in HDL that were induced by the acute-phase response. The acute-phase response is a systemic reaction to infectious and noninfectious tissue-destructive processes. Unlike LDL, HDL is chameleon-like, changing its colors (apoproteins and associated enzymes) as the landscape changes (going from the basal state to the acute-phase response and back to the basal state). If HDL protection is largely due to its ability to inhibit or destroy the biologically active lipids in mildly oxidized LDL, the changes in HDL induced by the acute-phase response could result in an increase in the local modification (oxidation) of LDL in the artery wall. Consequently, monocyte infiltration at such sites may increase during an acute-phase response. The major site of monocyte entry into lipid-rich plaques that are prone to rupture is at the shoulder region of lesions, and the major determinant of plaque rupture appears to be the intensity of monocyte infiltration at such sites.

In this issue factors including nutritional habits, physical activity, good sleep, stress management and HDL in menopause will be covered.

Prof. Dr. Mohamad Navab
Guest Editor

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Keywords

  • nutrition and HDL
  • physical activity and HDL
  • sleep and HDL
  • stress and HDL
  • genetics and HDL
  • therapeutic approach to HDL abnormality
  • dysfunctional HDL
  • HDL levels vs HDL function

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Published Papers (3 papers)

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Research

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12 pages, 1259 KiB  
Article
Sphingosine 1-Phosphate and Apolipoprotein M Levels and Their Correlations with Inflammatory Biomarkers in Patients with Untreated Familial Hypercholesterolemia
by Lilla Juhász, Hajnalka Lőrincz, Anita Szentpéteri, Bíborka Nádró, Éva Varga, György Paragh and Mariann Harangi
Int. J. Mol. Sci. 2022, 23(22), 14065; https://doi.org/10.3390/ijms232214065 - 15 Nov 2022
Cited by 4 | Viewed by 1667
Abstract
High-density lipoprotein (HDL)-bound apolipoprotein M/sphingosine 1-phosphate (ApoM/S1P) complex in cardiovascular diseases serves as a bridge between HDL and endothelial cells, maintaining a healthy endothelial barrier. To date, S1P and ApoM in patients with untreated heterozygous familial hypercholesterolemia (HeFH) have not been extensively studied. [...] Read more.
High-density lipoprotein (HDL)-bound apolipoprotein M/sphingosine 1-phosphate (ApoM/S1P) complex in cardiovascular diseases serves as a bridge between HDL and endothelial cells, maintaining a healthy endothelial barrier. To date, S1P and ApoM in patients with untreated heterozygous familial hypercholesterolemia (HeFH) have not been extensively studied. Eighty-one untreated patients with HeFH and 32 healthy control subjects were included in this study. Serum S1P, ApoM, sCD40L, sICAM-1, sVCAM-1, oxLDL, and TNFα concentrations were determined by ELISA. PON1 activities were measured spectrophotometrically. Lipoprotein subfractions were detected by Lipoprint. We diagnosed FH using the Dutch Lipid Clinic Network criteria. Significantly higher serum S1P and ApoM levels were found in HeFH patients compared to controls. S1P negatively correlated with large HDL and positively with small HDL subfractions in HeFH patients and the whole study population. S1P showed significant positive correlations with sCD40L and MMP-9 levels and PON1 arylesterase activity, while we found significant negative correlation between sVCAM-1 and S1P in HeFH patients. A backward stepwise multiple regression analysis showed that the best predictors of serum S1P were large HDL subfraction and arylesterase activity. Higher S1P and ApoM levels and their correlations with HDL subfractions and inflammatory markers in HeFH patients implied their possible role in endothelial protection. Full article
(This article belongs to the Special Issue High-Density Lipoprotein in Cardiovascular Disease)
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Review

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32 pages, 1089 KiB  
Review
The Role of Selected lncRNAs in Lipid Metabolism and Cardiovascular Disease Risk
by Anna Gluba-Sagr, Beata Franczyk, Aleksandra Rysz-Górzyńska, Robert Olszewski and Jacek Rysz
Int. J. Mol. Sci. 2024, 25(17), 9244; https://doi.org/10.3390/ijms25179244 - 26 Aug 2024
Viewed by 1065
Abstract
Lipid disorders increase the risk for the development of cardiometabolic disorders, including type 2 diabetes, atherosclerosis, and cardiovascular disease. Lipids levels, apart from diet, smoking, obesity, alcohol consumption, and lack of exercise, are also influenced by genetic factors. Recent studies suggested the role [...] Read more.
Lipid disorders increase the risk for the development of cardiometabolic disorders, including type 2 diabetes, atherosclerosis, and cardiovascular disease. Lipids levels, apart from diet, smoking, obesity, alcohol consumption, and lack of exercise, are also influenced by genetic factors. Recent studies suggested the role of long noncoding RNAs (lncRNAs) in the regulation of lipid formation and metabolism. Despite their lack of protein-coding capacity, lncRNAs are crucial regulators of various physiological and pathological processes since they affect the transcription and epigenetic chromatin remodelling. LncRNAs act as molecular signal, scaffold, decoy, enhancer, and guide molecules. This review summarises available data concerning the impact of lncRNAs on lipid levels and metabolism, as well as impact on cardiovascular disease risk. This relationship is significant because altered lipid metabolism is a well-known risk factor for cardiovascular diseases, and lncRNAs may play a crucial regulatory role. Understanding these mechanisms could pave the way for new therapeutic strategies to mitigate cardiovascular disease risk through targeted modulation of lncRNAs. The identification of dysregulated lncRNAs may pose promising candidates for therapeutic interventions, since strategies enabling the restoration of their levels could offer an effective means to impede disease progression without disrupting normal biological functions. LncRNAs may also serve as valuable biomarker candidates for various pathological states, including cardiovascular disease. However, still much remains unknown about the functions of most lncRNAs, thus extensive studies are necessary elucidate their roles in physiology, development, and disease. Full article
(This article belongs to the Special Issue High-Density Lipoprotein in Cardiovascular Disease)
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14 pages, 1808 KiB  
Review
Air Pollution: Another Threat to HDL Function
by Alice Ossoli, Federica Cetti and Monica Gomaraschi
Int. J. Mol. Sci. 2023, 24(1), 317; https://doi.org/10.3390/ijms24010317 - 24 Dec 2022
Cited by 11 | Viewed by 2674
Abstract
Epidemiological studies have consistently demonstrated a positive association between exposure to air pollutants and the incidence of cardiovascular disease, with the strongest evidence for particles with a diameter < 2.5 μm (PM2.5). Therefore, air pollution has been included among the modifiable [...] Read more.
Epidemiological studies have consistently demonstrated a positive association between exposure to air pollutants and the incidence of cardiovascular disease, with the strongest evidence for particles with a diameter < 2.5 μm (PM2.5). Therefore, air pollution has been included among the modifiable risk factor for cardiovascular outcomes as cardiovascular mortality, acute coronary syndrome, stroke, heart failure, and arrhythmias. Interestingly, the adverse effects of air pollution are more pronounced at higher levels of exposure but were also shown in countries with low levels of air pollution, indicating no apparent safe threshold. It is generally believed that exposure to air pollution in the long-term can accelerate atherosclerosis progression by promoting dyslipidemia, hypertension, and other metabolic disorders due to systemic inflammation and oxidative stress. Regarding high density lipoproteins (HDL), the impact of air pollution on plasma HDL-cholesterol levels is still debated, but there is accumulating evidence that HDL function can be impaired. In particular, the exposure to air pollution has been variably associated with a reduction in their cholesterol efflux capacity, antioxidant and anti-inflammatory potential, and ability to promote the release of nitric oxide. Further studies are needed to fully address the impact of various air pollutants on HDL functions and to elucidate the mechanisms responsible for HDL dysfunction. Full article
(This article belongs to the Special Issue High-Density Lipoprotein in Cardiovascular Disease)
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