HDL cholesterol efflux capacity and cardiovascular mortality

Ritsch, Andreas; Duerr, A.; Kahler, Patrick; Stojaković, Tatjana; Silbernagel, Günther; Scharnagl, Hubert; Kleber, Marcus E.; März, Winfried

doi:10.1016/j.atherosclerosis.2015.04.106

Cited by 8 publications

(11 citation statements)

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“…showed that cholesterol efflux in patients of the Dallas Heart Study was inversely associated with the incidence of cardiovascular events . We have recently extended this work to patients at high risk for cardiovascular disease by showing an inverse association between cholesterol efflux capacity and cardiovascular mortality . Pomegranate extracts are containing significant amounts of ellagitannins as their major bioactive phenolic compounds, which are turned into low‐molecular weight compounds including urolithin B by components of the gut microbiota.…”

Section: Discussionmentioning

confidence: 92%

“…We are aware that measurement of cholesterol efflux capacity does not reflect the whole reverse cholesterol transport. However, cholesterol efflux is the first major step within this pathway and the technology used has been shown to be useful in several clinical studies by us and others . Accordingly, we measured efflux capacity of apoB‐depleted plasma containing primarily HDL from coronary artery disease patients.…”

Section: Discussionmentioning

confidence: 99%

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A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE^−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

Zhao

Wang

Haller

et al. 2019

Molecular Nutrition Food Res

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Scope: HDL cholesterol is inversely related to the incidence of atherosclerosis. Polyphenols including ellagitannins have been shown to exert antiatherogenic properties. Urolithin B is formed from ellagitannins by components of the gut microbiota, and urolithins might be involved in beneficial effects against cardiovascular diseases in vitro. In this study, the influence of urolithin B on several parameters involved in the lipid plaque deposition and the reverse cholesterol transport is investigated. Methods and results: In apoE −/− mice and two different macrophage cell lines, the influence of urolithin B and its phase II conjugated metabolite on lipid plaque deposition, cholesterol uptake, and expression of ABCA1 and SR-BI is tested. It is shown that urolithin B decreases lipid plaque deposition, both urolithin B and urolithin B sulfate modulate expression of SR-BI and ABCA1, and cholesterol efflux increases from cholesterol laden macrophages to HDL particles as well as to reverse lipid uptake by stimulatedTHP-1 macrophages. Conclusions: Urolithin B can decrease lipid plaque deposition, and urolithin B and urolithin B sulfate are able to induce reverse cholesterol transport by influencing expression of key proteins of this pathway. Urolithin B may represent the basis for development of new drugs for prevention and treatment of atherosclerosis in humans.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE^−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

Zhao

Wang

Haller

et al. 2019

Molecular Nutrition Food Res

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“…Cholesterol efflux capacity (CEC) can vary by a factor of two at a given concentration of HDL-C. Thus far, several studies have used CEC [6,7]. In contrast to HDL-C, CEC is inversely correlated to CVD risk and low CEC is an independent risk factor for CVD.…”

Section: Lipids and Cvd (Cardiovascular Disease) Riskmentioning

confidence: 99%

What are the prospects of apolipoprotein profiling for cardiovascular disease?

Baig

Mayr

2017

Expert Review of Molecular Diagnostics

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“…HDL cholesterol efflux capacity was quantified using a validated ex vivo assay that measures the ability of apolipoprotein-B depleted serum to mobilize cholesterol from cholesterol-laden macrophages [23,[28][29][30][31]. J774 cells, a mouse macrophage cell line [32], were plated and labeled for 24 hours with 1 μCi/mL Hcholesterol efflux was determined by incubating cells with 2.8% apoB-depleted serum for 4 hours as described [28].…”

Section: Measurements Of Hdl Cholesterol Efflux Capacitymentioning

confidence: 99%

Metrics of high-density lipoprotein function and hospital mortality in acute heart failure patients

et al. 2016

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ObjectiveThe functionality of high-density lipoprotein (HDL) is impaired in chronic ischaemic heart failure (HF). However, the relationship between HDL functionality and outcomes in acute HF (AHF) has not been studied. The present study investigates whether the metrics of HDL functionality, including HDL cholesterol efflux capacity and HDL-associated paraoxonase (PON)-1 arylesterase (AE) activity are associated with hospital mortality in AHF patients. Methods and ResultsThe study was performed as a prospective, single-centre, observational research on 152 patients, defined and categorised according to the ESC and ACCF/AHA Guidelines for HF by time of onset, final clinical presentation and ejection fraction. The mean age of the included patients (52% female) was 75.2 years (SD 10.3) and hospital mortality was 14.5%. HDL cholesterol efflux capacity was examined by measuring the capacity of apoB depleted serum to remove tritium-labelled cholesterol from cultured macrophages. The AE activity of the HDL fraction was examined by a photometric assay. In a univariable regression analysis, low cholesterol efflux, but not AE activity, was significantly associated with hospital mortality [odds ratio (OR) 0.78, 95% confidence interval (CI) 0.64-0.96, p = 0.019]. In multivariable analysis progressively adjusting for important clinical and laboratory parameters the association obtained for cholesterol efflux capacity and hospital mortality by univariable analysis, despite a stable OR, did not stay significant (p = 0.179). ConclusionOur results suggest that HDL cholesterol efflux capacity (but not AE activity) contributes to, but is not an independent risk factor for, hospital mortality in AHF patients. Larger studies are needed to draw firm conclusions.

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HDL cholesterol efflux capacity and cardiovascular mortality

Cited by 8 publications

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A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE^−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE^−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

What are the prospects of apolipoprotein profiling for cardiovascular disease?

Metrics of high-density lipoprotein function and hospital mortality in acute heart failure patients

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HDL cholesterol efflux capacity and cardiovascular mortality

Cited by 8 publications

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A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

What are the prospects of apolipoprotein profiling for cardiovascular disease?

Metrics of high-density lipoprotein function and hospital mortality in acute heart failure patients

Contact Info

Product

Resources

About

A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE^−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells

A Novel Candidate for Prevention and Treatment of Atherosclerosis: Urolithin B Decreases Lipid Plaque Deposition in apoE^−/− Mice and Increases Early Stages of Reverse Cholesterol Transport in ox‐LDL Treated Macrophages Cells