Glycosylation of HDL-Associated Proteins and Its Implications in Cardiovascular Disease Diagnosis, Metabolism and Function

Romo, Eduardo Z.; Zivkovic, Angela M.

doi:10.3389/fcvm.2022.928566

Cited by 4 publications

(3 citation statements)

References 134 publications

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“…The observed association could be an epiphenomenon driven by a pathophysiologic abnormality, perhaps immunologic, genetic, and epigenetic, which increases cardiovascular risk in ways we do not fully understand yet and also increases HDL, substantiating the complexity of HDL-C pathobiology. [50][51][52][53][54] Conformation and functional properties of HDL particles 55,56 may also be altered in individuals with extreme high HDL-C and an alternative hypothesis could be that in individuals with particularly high HDL-C levels, the functionality of HDL may be compromised such that HDL does not function properly but rather becomes detrimental.…”

Section: Discussionmentioning

confidence: 99%

High HDL (High-Density Lipoprotein) Cholesterol Increases Cardiovascular Risk in Hypertensive Patients

et al. 2022

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Background: Emerging evidence suggests that elevated circulating levels of HDL-C (high-density lipoprotein cholesterol) could be linked to an increased mortality risk. However, to the best of our knowledge, the relationship between HDL-C and specific cardiovascular events has never been investigated in patients with hypertension. Methods: To fill this knowledge gap, we analyzed the relationship between HDL-C levels and cardiovascular events in hypertensive patients within the Campania Salute Network in Southern Italy. Results: We studied 11 987 patients with hypertension, who were followed for 25 534 person-years. Our population was divided in 3 groups according to the HDL-C plasma levels: HDL-C<40 mg/dL (low HDL-C); HDL-C between 40 and 80 mg/dL (medium HDL-C); and HDL-C>80 mg/dL (high HDL-C). At the follow-up analysis, adjusting for potential confounders, we observed a total of 245 cardiovascular events with a significantly increased risk of cardiovascular events in the low HDL-C group and in the high HDL-C arm compared with the medium HDL-C group. The spline analysis revealed a nonlinear U-shaped association between HDL-C levels and cardiovascular outcomes. Interestingly, the increased cardiovascular risk associated with high HDL-C was not confirmed in female patients. Conclusions: Our data demonstrate that there is a U-shaped association between HDL-C and the risk of cardiovascular events in male patients with hypertension.

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Section: Discussionmentioning

confidence: 99%

High HDL (High-Density Lipoprotein) Cholesterol Increases Cardiovascular Risk in Hypertensive Patients

et al. 2022

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“…Given the significance of HDL glycosylation in its function, exploring therapeutic approaches to enhance function by modulating glycosylation is a captivating area of research [135]. Understanding the role of glycosylation in HDL particles could open new opportunities for improving their function and potentially benefitting human health by interventions such as diet and exercise.…”

Section: Hdl Glycosylationmentioning

confidence: 99%

Precision Nutrition and Cardiovascular Disease Risk Reduction: the Promise of High-Density Lipoproteins

Hong,

Agus,

Tang

et al. 2023

Curr Atheroscler Rep

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Purpose of Review Emerging evidence supports the promise of precision nutritional approaches for cardiovascular disease (CVD) prevention. Here, we discuss current findings from precision nutrition trials and studies reporting substantial inter-individual variability in responses to diets and dietary components relevant to CVD outcomes. We highlight examples where early precision nutrition research already points to actionable intervention targets tailored to an individual’s biology and lifestyle. Finally, we make the case for high-density lipoproteins (HDL) as a compelling next generation target for precision nutrition aimed at CVD prevention. HDL possesses complex structural features including diverse protein components, lipids, size distribution, extensive glycosylation, and interacts with the gut microbiome, all of which influence HDL’s anti-inflammatory, antioxidant, and cholesterol efflux properties. Elucidating the nuances of HDL structure and function at an individual level may unlock personalized dietary and lifestyle strategies to optimize HDL-mediated atheroprotection and reduce CVD risk. Recent Findings Recent human studies have demonstrated that HDL particles are key players in the reduction of CVD risk. Our review highlights the role of HDL and the importance of personalized therapeutic approaches to improve their potential for reducing CVD risk. Factors such as diet, genetics, glycosylation, and gut microbiome interactions can modulate HDL structure and function at the individual level. We emphasize that fractionating HDL into size-based subclasses and measuring particle concentration are necessary to understand HDL biology and for developing the next generation of diagnostics and biomarkers. These discoveries underscore the need to move beyond a one-size-fits-all approach to HDL management. Precision nutrition strategies that account for personalized metabolic, genetic, and lifestyle data hold promise for optimizing HDL therapies and function to mitigate CVD risk more potently. Summary While human studies show HDL play a key role in reducing CVD risk, recent findings indicate that factors such as diet, genetics, glycosylation, and gut microbes modulate HDL function at the individual level, underscoring the need for precision nutrition strategies that account for personalized variability to optimize HDL’s potential for mitigating CVD risk.

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“…High-density lipoproteins (HDL) are heterogenous nanoparticles most commonly known for their role in cholesterol homeostasis but they also play a critical role in modulating TLR4-based inflammatory responses along with LBP by trafficking, neutralizing and clearing LPS (26,27). Recent findings indicate that HDL synthesized in the intestinal tract bind LBP to regulate LPS -mediated activation of liver inflammation (28).…”

Section: Introductionmentioning

confidence: 99%

Elevated lipopolysaccharide binding protein in Alzheimer’s disease patients with APOE3/E3 but not APOE3/E4 genotype

Romo,

Hong,

Patel

et al. 2024

Front. Neurol.

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IntroductionThe role of lipopolysaccharide binding protein (LBP), an inflammation marker of bacterial translocation from the gastrointestinal tract, in Alzheimer’s disease (AD) is not clearly understood.MethodsIn this study the concentrations of LBP were measured in n = 79 individuals: 20 apolipoprotein E (APOE)3/E3 carriers with and 20 without AD dementia, and 19 APOE3/E4 carriers with and 20 without AD dementia. LBP was found to be enriched in the 1.21–1.25 g/mL density fraction of plasma, which has previously been shown to be enriched in intestinally derived high-density lipoproteins (HDL). LBP concentrations were measured by ELISA.ResultsLBP was significantly increased within the 1.21–1.25 g/mL density fraction of plasma in APOE3/E3 AD patients compared to controls, but not APOE3/E4 patients. LBP was positively correlated with Clinical Dementia Rating (CDR) and exhibited an inverse relationship with Verbal Memory Score (VMS).DiscussionThese results underscore the potential contribution of gut permeability to bacterial toxins, measured as LBP, as an inflammatory mediator in the development of AD, particularly in individuals with the APOE3/E3 genotype, who are genetically at 4-12-fold lower risk of AD than individuals who express APOE4.

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Glycosylation of HDL-Associated Proteins and Its Implications in Cardiovascular Disease Diagnosis, Metabolism and Function

Cited by 4 publications

References 134 publications

High HDL (High-Density Lipoprotein) Cholesterol Increases Cardiovascular Risk in Hypertensive Patients

High HDL (High-Density Lipoprotein) Cholesterol Increases Cardiovascular Risk in Hypertensive Patients

Precision Nutrition and Cardiovascular Disease Risk Reduction: the Promise of High-Density Lipoproteins

Elevated lipopolysaccharide binding protein in Alzheimer’s disease patients with APOE3/E3 but not APOE3/E4 genotype

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