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Hypercholesterolemia: HELP
Articles by Ulf Landmesser
Based on 12 articles published since 2010
(Why 12 articles?)
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Between 2010 and 2020, U. Landmesser wrote the following 12 articles about Hypercholesterolemia.
 
+ Citations + Abstracts
1 Guideline New AHA and ACC guidelines on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk. 2014

Klose, Gerald / Beil, Frank Ulrich / Dieplinger, Hans / von Eckardstein, Arnold / Föger, Bernhard / Gouni-Berthold, Ioanna / Heigl, Franz / Koenig, Wolfgang / Kostner, Gert M / Landmesser, Ulf / Laufs, Ulrich / Leistikow, Frank / März, Winfried / Noll, Georg / Parhofer, Klaus G / Paulweber, Bernhard / Riesen, Walter F / Schaefer, Jürgen R / Steinhagen-Thiessen, Elisabeth / Steinmetz, Armin / Toplak, Hermann / Wanner, Christoph / Windler, Eberhard / Anonymous4800787. ·Practice for Internal Medicine, Gastroenterology, Cardiology and Preventive Medicine, Bremen, Germany. ·Wien Klin Wochenschr · Pubmed #24615676.

ABSTRACT: After the publication of the new guidelines of the European Society of Cardiology and the European Atherosclerosis Society for the prevention and treatment of dyslipidemias (Eur Heart J 32:1769-1818, 2011; Eur Heart J 33:1635-1701, 2012), a group of authors has recently published on behalf of the American Heart Association and the American College of Cardiology guidelines on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk (Circulation 2013). These new guidelines are supposed to replace the until now widely accepted, at least in the USA, recommendations of the National Cholesterol Education Program Adult Treatment Panel III from the years 2002 (Circulation 106:3143-3421, 2002) and 2004 (Circulation 110:227-39, 2004). Furthermore, they claim to be based mainly on hard evidence derived from the interpretation of results of prospective randomized controlled trials. This Joint Position Statement of the Society for the Prevention of Cardiovascular Diseases e.V. (D.A.CH), the Austrian Atherosclerosis Society and the Working Group on Lipids and Atherosclerosis (AGLA) of the Swiss Society of Cardiology concludes that the use of individualized prevention strategies based on specific indications and LDL cholesterol target concentrations, a strategy whose worth has been widely proven and accepted for more than a decade in Europe, should not be given up.

2 Review [Dyslipidemias : Diagnostics and management]. 2017

Sinning, D / Landmesser, U. ·Klinik für Kardiologie, Charité Centrum für Herz‑, Kreislauf- und Gefäßmedizin, Charité - Universitätsmedizin Berlin (Campus Benjamin Franklin), Hindenburgdamm 30, 12203, Berlin, Deutschland. · Klinik für Kardiologie, Charité Centrum für Herz‑, Kreislauf- und Gefäßmedizin, Charité - Universitätsmedizin Berlin (Campus Benjamin Franklin), Hindenburgdamm 30, 12203, Berlin, Deutschland. ulf.landmesser@charite.de. · Berlin Institute of Health (BIH), Berlin, Deutschland. ulf.landmesser@charite.de. · Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK), Berlin, Deutschland. ulf.landmesser@charite.de. ·Herz · Pubmed #28791432.

ABSTRACT: For disorders of lipid metabolism the risk-adapted adjustment of low-density lipoprotein (LDL) cholesterol remains the primary treatment target, as a causal role in minimizing the progression of ACVD has been shown. Because of their efficacy in reducing cardiovascular morbidity and mortality, statins are recommended as first-line pharmacological treatment in dyslipidemias. Additionally, ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition have been shown to significantly reduce cardiovascular events in high-risk patients. Life style changes can improve the plasma lipid profile, particularly in the setting of hypertriglyceridemia. Evaluation of high-density lipoprotein (HDL) cholesterol and lipoprotein(a) provides further information when assessing the individual cardiovascular risk, but direct evidence that pharmacologically targeting HDL cholesterol or Lp(a) results in a reduction of cardiovascular events has not yet been shown.

3 Review LDL-Cholesterol: Standards of Treatment 2016: A German Perspective. 2016

März, Winfried / Scharnagl, Hubert / Gouni-Berthold, Ioanna / Silbernagel, Günther / Dressel, Alexander / Grammer, Tanja B / Landmesser, Ulf / Dieplinger, Hans / Windler, Eberhard / Laufs, Ulrich. ·Society for the Prevention of Cardiovascular Disease e.V. (DACH), Schulterblatt 120, 20357, Hamburg, Germany. winfried.maerz@synlab.com. · Synlab Academy, Synlab Holding Germany GmbH, P5, 7, 68167, Mannheim, Germany. winfried.maerz@synlab.com. · Clinical Institut for Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Auenbrugger Platz, 8036, Graz, Austria. winfried.maerz@synlab.com. · Medical Clinic V (Nephrology, Hypertension, Rheumatology, Endocrinology, Diabetology), Mannheim Medical Faculty, University of Heidelberg, Ludolf Krehl Street 7-11, 68167, Mannheim, Germany. winfried.maerz@synlab.com. · Clinical Institut for Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Auenbrugger Platz, 8036, Graz, Austria. · Center for Endocrinology, Diabetes and Preventive Medicine, University of Cologne, Cologne, Germany. · Department of Angiology, Swiss Cardiovascular Center, University of Bern, Bern, Switzerland. · Society for the Prevention of Cardiovascular Disease e.V. (DACH), Schulterblatt 120, 20357, Hamburg, Germany. · Mannheimer Institute for Public Health, Mannheim Medical Faculty, University of Heidelberg, Heidelberg, Germany. · Clinic for Cardiology, Charité Medical University, Berlin, Germany. · Division of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria. · Preventive Medicine, Clinic and Policlinic for General and Invasive Cardiology, Univerity Heart Center Hamburg, University Clinic Hamburg-Eppendorf, Hamburg, Germany. · Clinic for Internal Medicine III (Cardiology, Angiology and Medical Intensive Care), University of Saarland, Homburg, Germany. ·Am J Cardiovasc Drugs · Pubmed #27430233.

ABSTRACT: Decreasing low-density lipoprotein cholesterol (LDL-C) is one of the few established and proven principles for the prevention and treatment of atherosclerosis. The higher the individual cardiovascular risk, the higher the benefit of lipid-lowering pharmacotherapy. Therefore, treatment options are chosen based on a patient's total cardiovascular risk. The latter depends not only on the levels of LDL-C but also on the presence of cardiovascular disease (CVD) and on the number and severity of other risk factors. Current guidelines recommend the lowering of LDL-C to 115 mg/dl (3 mmol/l) in patients with low and moderate risk. The LDL-C treatment target is <100 mg/dl (2.6 mmol/l) for patients at high risk and <70 mg/dl (1.8 mmol/l) for patients at very high risk. Although lifestyle measures remain a fundamental part of treatment, many patients require drug therapy to achieve their LDL-C targets. Statins are the drugs of choice, with other options including ezetimibe and the newly available monoclonal antibodies against PCSK9 (proprotein convertase subtilisin/kexin type 9). In some cases, bile acid-binding sequestrants and fibrates can also be considered. Nicotinic acid is no longer available in Germany. PCSK9 antibodies decrease LDL-C about 50-60 % and are well tolerated. Their effects on clinical endpoints are being investigated in large randomized trials. The aim of the present review is to summarize the current guidelines and treatment options for hypercholesterolemia. Moreover, we provide an appraisal of PCSK9 antibodies and propose their use in selected patient populations, particularly in those at very high cardiovascular risk whose LDL-C levels under maximally tolerated lipid-lowering therapy are significantly over their treatment target.

4 Review The year in cardiology 2015: prevention. 2016

Chapman, M John / Blankenberg, Stefan / Landmesser, Ulf. ·National Institute for Health and Medical Research (INSERM), Dyslipidemia and Atherosclerosis Research, Pitié-Salpêtrière University Hospital, Paris FR-75651, France University of Pierre and Marie Curie, Paris, France john.chapman@upmc.fr. · Clinic for Cardiology, University Heart Center Hamburg, German Center for Cardiovascular Research (DZHK), Hamburg, Germany. · Department of Cardiology, Charité Universitätsmedizin Berlin (CBF), Berlin, Germany German Center for Cardiovascular Research (DZHK), Berlin Institute of Health (BIH), Berlin, Germany. ·Eur Heart J · Pubmed #26726043.

ABSTRACT: -- No abstract --

5 Review High-density lipoprotein: vascular protective effects, dysfunction, and potential as therapeutic target. 2014

Lüscher, Thomas F / Landmesser, Ulf / von Eckardstein, Arnold / Fogelman, Alan M. ·From Department of Cardiology, University Heart Center (T.F.L., U.L.), and Department of Clinical Chemistry (A.v.E.), University Hospital Zurich, Zurich, Switzerland · Division of Cardiovascular Research, Institute of Physiology, University of Zurich, Zurich, Switzerland (T.F.L., U.L.) · and Department of Medicine, University of California, Los Angeles, CA (A.M.F.). ·Circ Res · Pubmed #24385510.

ABSTRACT: High-density lipoprotein (HDL) is a complex mixture of lipoproteins that is associated with many minor proteins and lipids that influence the function of HDL. Although HDL is a promising marker and potential therapeutic target based on its epidemiological data and the effects of healthy HDL in vitro in endothelial cells and macrophages, as well as based on infusion studies of reconstituted HDL in patients with hypercholesterolemia, it remains still uncertain whether or not HDL cholesterol-raising drugs will improve outcomes. Recent studies suggest that HDL becomes modified in patients with coronary artery disease or acute coronary syndrome because of oxidative processes that result in alterations in its proteome composition (proteome remodelling) leading to HDL dysfunction.

6 Review The Year in Cardiology 2013: cardiovascular disease prevention. 2014

Gielen, S / Landmesser, U. ·Department of Internal Medicine III, Martin-Luther-University Halle/Wittenberg, University Hospital, Ernst-Grube-Str. 40, 06120 Halle/Saale, Germany. ·Eur Heart J · Pubmed #24385374.

ABSTRACT: The decline in cardiovascular mortality in Europe by nearly 50% over the last three decades resulted in particular from improved risk factor control and prevention interventions in addition to improved treatment. This review provides an overview of key studies in epidemiology, hypertension control, lipidology, diabetology, and lifestyle changes published in 2013. EXAMINE in diabetology and AIM-High and HPS-2-THRIVE in lipidology failed to demonstrate an event reduction. According to EUROASPIRE IV clinical implementation of secondary prevention treatments is still suboptimal. The 2013 study highlights in prevention prove the dynamic progress of knowledge in the field;, however, knowledge alone is futile without implementation.

7 Clinical Trial Inclisiran in Patients at High Cardiovascular Risk with Elevated LDL Cholesterol. 2017

Ray, Kausik K / Landmesser, Ulf / Leiter, Lawrence A / Kallend, David / Dufour, Robert / Karakas, Mahir / Hall, Tim / Troquay, Roland P T / Turner, Traci / Visseren, Frank L J / Wijngaard, Peter / Wright, R Scott / Kastelein, John J P. ·From the Imperial Centre for Cardiovascular Disease Prevention, Department of Primary Care and Public Health, Imperial College London, London (K.K.R.), and Knowle House Surgery, Plymouth (T.H.) - both in the United Kingdom · the Department of Cardiology, Charité-Universitätsmedizin Berlin, Berlin Institute of Health and German Center for Cardiovascular Research, Berlin (U.L.), and University Heart Center Hamburg, Department of General and Interventional Cardiology, Hamburg (M.K.) - all in Germany · the Division of Endocrinology and Metabolism, Li Ka Shing Knowledge Institute and Keenan Research Centre for Biomedical Science, St. Michael's Hospital, University of Toronto, Toronto (L.A.L.) · the Medicines Company, Parsippany, NJ (D.K., P.W.) · Institut de Recherches Cliniques de Montréal, University of Montreal, Montreal (R.D.) · the Department of Cardiology and Interventional Cardiology, VieCuri Medical Center for Northern Limburg, Venlo (R.P.T.T.), University Medical Center, Utrecht (F.L.J.V.), and the Department of Vascular Medicine, Academic Medical Center-University of Amsterdam, Amsterdam (J.J.P.K.) - all in the Netherlands · the Metabolic and Atherosclerosis Research Center, Medpace, Cincinnati (T.T.) · and the Department of Cardiology, Mayo Clinic, Rochester, MN (R.S.W.). ·N Engl J Med · Pubmed #28306389.

ABSTRACT: BACKGROUND: In a previous study, a single injection of inclisiran, a chemically synthesized small interfering RNA designed to target PCSK9 messenger RNA, was found to produce sustained reductions in low-density lipoprotein (LDL) cholesterol levels over the course of 84 days in healthy volunteers. METHODS: We conducted a phase 2, multicenter, double-blind, placebo-controlled, multiple-ascending-dose trial of inclisiran administered as a subcutaneous injection in patients at high risk for cardiovascular disease who had elevated LDL cholesterol levels. Patients were randomly assigned to receive a single dose of placebo or 200, 300, or 500 mg of inclisiran or two doses (at days 1 and 90) of placebo or 100, 200, or 300 mg of inclisiran. The primary end point was the change from baseline in LDL cholesterol level at 180 days. Safety data were available through day 210, and data on LDL cholesterol and proprotein convertase subtilisin-kexin type 9 (PCSK9) levels were available through day 240. RESULTS: A total of 501 patients underwent randomization. Patients who received inclisiran had dose-dependent reductions in PCSK9 and LDL cholesterol levels. At day 180, the least-squares mean reductions in LDL cholesterol levels were 27.9 to 41.9% after a single dose of inclisiran and 35.5 to 52.6% after two doses (P<0.001 for all comparisons vs. placebo). The two-dose 300-mg inclisiran regimen produced the greatest reduction in LDL cholesterol levels: 48% of the patients who received the regimen had an LDL cholesterol level below 50 mg per deciliter (1.3 mmol per liter) at day 180. At day 240, PCSK9 and LDL cholesterol levels remained significantly lower than at baseline in association with all inclisiran regimens. Serious adverse events occurred in 11% of the patients who received inclisiran and in 8% of the patients who received placebo. Injection-site reactions occurred in 5% of the patients who received injections of inclisiran. CONCLUSIONS: In our trial, inclisiran was found to lower PCSK9 and LDL cholesterol levels among patients at high cardiovascular risk who had elevated LDL cholesterol levels. (Funded by the Medicines Company; ORION-1 ClinicalTrials.gov number, NCT02597127 .).

8 Article Reduction of low density lipoprotein-cholesterol and cardiovascular events with proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors and statins: an analysis of FOURIER, SPIRE, and the Cholesterol Treatment Trialists Collaboration. 2018

Ference, Brian A / Cannon, Christopher P / Landmesser, Ulf / Lüscher, Thomas F / Catapano, Alberico L / Ray, Kausik K. ·Division of Translational Research and Clinical Epidemiology, Division of Cardiovascular Medicine, Wayne State University School of Medicine, Detroit, MI, USA. · Cardiovascular Division, Brigham and Women's Hospital, Boston, MA, USA. · Department of Cardiology, Charite Universitäts Medizin Berlin, Campus Benjamin Franklin, Berlin, Germany. · Department of Cardiology, University Heart Center, University Hospital Zurich, Switzerland. · Department of Pharmacological and Biomolecular Sciences, MultiMedica Istituto di Ricovero e Cura a Carattere Scientifico, University of Milan, Via Balzaretti, 9, 20133 Milan, Italy. · Imperial Centre for Cardiovascular Disease Prevention, Department of Primary Care and Public Health, School of Public Health, Imperial College, London, UK. ·Eur Heart J · Pubmed #29020411.

ABSTRACT: -- No abstract --

9 Article DPP-4 inhibition ameliorates atherosclerosis by priming monocytes into M2 macrophages. 2015

Brenner, C / Franz, W M / Kühlenthal, S / Kuschnerus, K / Remm, F / Gross, L / Theiss, H D / Landmesser, U / Kränkel, N. ·Department of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria; Department of Internal Medicine I, University of Munich, Munich, Germany. Electronic address: mail@med.cbrenner.net. · Department of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria. · Department of Internal Medicine I, University of Munich, Munich, Germany. · Center for Molecular Cardiology, University of Zurich, Zurich, Switzerland; Department of Cardiology, Charité - Universitätsmedizin Berlin, Berlin, Germany. · Department of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria; Department of Internal Medicine I, University of Munich, Munich, Germany. · Center for Molecular Cardiology, University of Zurich, Zurich, Switzerland; Department of Cardiology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Electronic address: nicolle.kraenkel@charite.de. ·Int J Cardiol · Pubmed #26197403.

ABSTRACT: OBJECTIVE: Glipitins are widely used for the treatment of type 2 diabetic patients. In addition to their improvement of glycemic control, animal studies have suggested an independent anti-atherosclerotic effect of gliptins. Nevertheless, recent clinical trials regarding long-term effects of gliptin therapy on vascular events have been disappointing. This discrepancy led us to better dissect the functional role of SDF-1/CXCR4 signaling as a potential mechanism underlying gliptin action. The study should give improved understanding of the potential of gliptin therapy in the prevention and treatment of atherosclerosis. METHODS AND RESULTS: In an ApoE-/- mouse model on high cholesterol diet, long-term treatment with the DPP-4 inhibitor Sitagliptin significantly reduced atherosclerosic plaque load in the aorta. Flow cytometry analyses showed an enrichment of M2 macrophages in the aortic wall under gliptin therapy. Importantly, the number of recruited CD206+ macrophages was inversely correlated with total plaque area while no correlation was found for the overall macrophage population or M1 macrophages. Blockade of CXCR4/SDF-1 signaling by AMD3100 inhibited aortic M2 accumulation and the therapeutic effect of Sitagliptin. Correspondingly, Sitagliptin shifted the polarization profile of macrophages towards a M2-like phenotype. CONCLUSION: Sitagliptin-mediated inhibition of early atherosclerosis is based on M2-polarization during monocyte differentiation via the SDF-1/CXCR4 signaling. In contrast to earlier assumptions gliptin treatment might be especially effective in prevention of atherosclerosis.

10 Article [New AHA and ACC guidelines on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk : Statement of the D•A•CH Society for Prevention of Cardiovascular Diseases, the Austrian Atherosclerosis Society and the Working Group on Lipids and Atherosclerosis (AGLA) of the Swiss Society for Cardiology]. 2014

Klose, G / Beil, F U / Dieplinger, H / von Eckardstein, A / Föger, B / Gouni-Berthold, I / Koenig, W / Kostner, G M / Landmesser, U / Laufs, U / Leistikow, F / März, W / Merkel, M / Müller-Wieland, D / Noll, G / Parhofer, K G / Paulweber, B / Riesen, W / Schaefer, J R / Steinhagen-Thiessen, E / Steinmetz, A / Toplak, H / Wanner, C / Windler, E. ·Praxis für Innere Medizin, Gastroenterologie, Kardiologie und Präventionsmedizin, Bremen, Deutschland. ·Internist (Berl) · Pubmed #24770979.

ABSTRACT: Guidelines for the reduction of cholesterol to prevent atherosclerotic vascular events were recently released by the American Heart Association and the American College of Cardiology. The authors claim to refer entirely to evidence from randomized controlled trials, thereby confining their guidelines to statins as the primary therapeutic option. The guidelines derived from these trials do not specify treatment goals, but refer to the percentage of cholesterol reduction by statin medication with low, moderate, and high intensity. However, these targets are just as little tested in randomized trials as are the cholesterol goals derived from clinical experience. The same applies to the guidelines of the four patient groups which are defined by vascular risk. No major statin trial has included patients on the basis of their global risk; thus the allocation criteria are also arbitrarily chosen. These would actually lead to a significant increase in the number of patients to be treated with high or maximum dosages of statins. Also, adhering to dosage regulations instead of cholesterol goals contradicts the principles of individualized patient care. The option of the new risk score to calculate lifetime risk up to the age of 80 years in addition to the 10-year risk can be appreciated. Unfortunately it is not considered in the therapeutic recommendations provided, despite evidence from population and genetic studies showing that even a moderate lifetime reduction of low-density lipoprotein (LDL) cholesterol or non-HDL cholesterol has a much stronger effect than an aggressive treatment at an advanced age. In respect to secondary prevention, the new American guidelines broadly match the European guidelines. Thus, the involved societies from Germany, Austria and Switzerland recommend continuing according to established standards, such as the EAS/ESC guidelines.

11 Article SIRT1 reduces endothelial activation without affecting vascular function in ApoE-/- mice. 2010

Stein, Sokrates / Schäfer, Nicola / Breitenstein, Alexander / Besler, Christian / Winnik, Stephan / Lohmann, Christine / Heinrich, Kathrin / Brokopp, Chad E / Handschin, Christoph / Landmesser, Ulf / Tanner, Felix C / Lüscher, Thomas F / Matter, Christian M. ·Cardiovascular Research, Institute of Physiology, Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, and Cardiovascular Center, Cardiology, University Hospital Zurich, CH-8057 Zurich, Switzerland. sokrates@access.uzh.ch ·Aging (Albany NY) · Pubmed #20606253.

ABSTRACT: Excessive production of reactive oxygen species (ROS) contributes to progression of atherosclerosis, at least in part by causing endothelial dysfunction and inflammatory activation. The class III histone deacetylase SIRT1 has been implicated in extension of lifespan. In the vasculature,SIRT1 gain-of-function using SIRT1 overexpression or activation has been shown to improve endothelial function in mice and rats via stimulation of endothelial nitric oxide (NO) synthase (eNOS). However, the effects of SIRT1 loss-of-function on the endothelium in atherosclerosis remain to be characterized. Thus, we have investigated the endothelial effects of decreased endogenous SIRT1 in hypercholesterolemic ApoE-/- mice. We observed no difference in endothelial relaxation and eNOS (Ser1177) phosphorylation between 20-week old male atherosclerotic ApoE-/- SIRT1+/- and ApoE-/- SIRT1+/+ mice. However, SIRT1 prevented endothelial superoxide production, inhibited NF-kappaB signaling, and diminished expression of adhesion molecules. Treatment of young hypercholesterolemic ApoE-/- SIRT1+/- mice with lipopolysaccharide to boost NF-kappaB signaling led to a more pronounced endothelial expression of ICAM-1 and VCAM-1 as compared to ApoE-/- SIRT1+/+ mice. In conclusion, endogenous SIRT1 diminishes endothelial activation in ApoE-/- mice, but does not affect endothelium-dependent vasodilatation.

12 Article SIRT1 decreases Lox-1-mediated foam cell formation in atherogenesis. 2010

Stein, Sokrates / Lohmann, Christine / Schäfer, Nicola / Hofmann, Janin / Rohrer, Lucia / Besler, Christian / Rothgiesser, Karin M / Becher, Burkhard / Hottiger, Michael O / Borén, Jan / McBurney, Michael W / Landmesser, Ulf / Lüscher, Thomas F / Matter, Christian M. ·Cardiovascular Research, Institute of Physiology, Zurich University and Cardiology, Cardiovascular Center, University Hospital Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland. ·Eur Heart J · Pubmed #20418343.

ABSTRACT: AIMS: Endothelial activation, macrophage infiltration, and foam cell formation are pivotal steps in atherogenesis. Our aim in this study was to analyse the role of SIRT1, a class III deacetylase with important metabolic functions, in plaque macrophages and atherogenesis. METHODS AND RESULTS: Using partial SIRT1 deletion in atherosclerotic mice, we demonstrate that SIRT1 protects against atherosclerosis by reducing macrophage foam cell formation. Peritoneal macrophages from heterozygous SIRT1 mice accumulate more oxidized low-density lipoprotein (oxLDL), thereby promoting foam cell formation. Bone marrow-restricted SIRT1 deletion confirmed that SIRT1 function in macrophages is sufficient to decrease atherogenesis. Moreover, we show that SIRT1 reduces the uptake of oxLDL by diminishing the expression of lectin-like oxLDL receptor-1 (Lox-1) via suppression of the NF-κB signalling pathway. CONCLUSION: Our findings demonstrate protective effects of SIRT1 in atherogenesis and suggest pharmacological SIRT1 activation as a novel anti-atherosclerotic strategy by reducing macrophage foam cell formation.