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Dr. Heidi Noels
RWTH University Hospital Aachen

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0 Atherosclerosis
0 Cardiovascular Disease
0 Inflammation
0 cardiorenal syndrome
0 Cellular Signalling

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Review article
Published: 10 May 2021 in Nature Reviews Nephrology
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Chronic kidney disease (CKD) induces modifications in lipid and lipoprotein metabolism and homeostasis. These modifications can promote, modulate and/or accelerate CKD and secondary cardiovascular disease (CVD). Lipid and lipoprotein abnormalities — involving triglyceride-rich lipoproteins, LDL and/or HDL — not only involve changes in concentration but also changes in molecular structure, including protein composition, incorporation of small molecules and post-translational modifications. These alterations modify the function of lipoproteins and can trigger pro-inflammatory and pro-atherogenic processes, as well as oxidative stress. Serum fatty acid levels are also often altered in patients with CKD and lead to changes in fatty acid metabolism — a key process in intracellular energy production — that induce mitochondrial dysfunction and cellular damage. These fatty acid changes might not only have a negative impact on the heart, but also contribute to the progression of kidney damage. The presence of these lipoprotein alterations within a biological environment characterized by increased inflammation and oxidative stress, as well as the competing risk of non-atherosclerotic cardiovascular death as kidney function declines, has important therapeutic implications. Additional research is needed to clarify the pathophysiological link between lipid and lipoprotein modifications, and kidney dysfunction, as well as the genesis and/or progression of CVD in patients with kidney disease. Chronic kidney disease (CKD) is associated with alterations in serum lipid profiles that contribute to kidney and cardiovascular disease. Here, the authors examine these changes in serum levels, metabolism and post-translational modifications of lipoproteins and fatty acids that characterize CKD-associated dyslipidaemia.

ACS Style

Heidi Noels; Michael Lehrke; Raymond Vanholder; Joachim Jankowski. Lipoproteins and fatty acids in chronic kidney disease: molecular and metabolic alterations. Nature Reviews Nephrology 2021, 1 -15.

AMA Style

Heidi Noels, Michael Lehrke, Raymond Vanholder, Joachim Jankowski. Lipoproteins and fatty acids in chronic kidney disease: molecular and metabolic alterations. Nature Reviews Nephrology. 2021; ():1-15.

Chicago/Turabian Style

Heidi Noels; Michael Lehrke; Raymond Vanholder; Joachim Jankowski. 2021. "Lipoproteins and fatty acids in chronic kidney disease: molecular and metabolic alterations." Nature Reviews Nephrology , no. : 1-15.

Review
Published: 03 May 2021 in Journal of the American Society of Nephrology
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Background Patients with CKD are at high risk for thrombotic and hemorrhagic complications. Abnormalities in platelet function are central to these complications, but reports on platelet function in relation to CKD are conflicting, and vary from decreased platelet reactivity to normal or increased platelet responsiveness. The direct effects of uremic toxins on platelet function have been described, with variable findings. Methods To help clarify how CKD affects platelet function, we conducted a systematic review and meta-analysis of platelet activity in CKD, with a focus on nondialysis-induced effects. We also performed an extensive literature search for the effects of individual uremic toxins on platelet function. Results We included 73 studies in the systematic review to assess CKD’s overall effect on platelet function in patients; 11 of them described CKD’s effect on ex vivo platelet aggregation and were included in the meta-analysis. Although findings on platelet abnormalities in CKD are inconsistent, bleeding time was mostly prolonged and platelet adhesion mainly reduced. Also, the meta-analysis revealed maximal platelet aggregation was significantly reduced in patients with CKD upon collagen stimulation. We also found that relatively few uremic toxins have been examined for direct effects on platelets ex vivo; ex vivo analyses had varying methods and results, revealing both platelet-stimulatory and inhibitory effects. However, eight of the 12 uremic toxins tested in animal models mostly induced prothrombotic effects. Conclusions Overall, most studies report impaired function of platelets from patients with CKD. Still, a substantial number of studies find platelet function to be unchanged or even enhanced. Further investigation of platelet reactivity in CKD, especially during different CKD stages, is warranted.

ACS Style

Constance C.F.M.J. Baaten; Marieke Sternkopf; Tobias Henning; Nikolaus Marx; Joachim Jankowski; Heidi Noels. Platelet Function in CKD: A Systematic Review and Meta-Analysis. Journal of the American Society of Nephrology 2021, 32, 1583 -1598.

AMA Style

Constance C.F.M.J. Baaten, Marieke Sternkopf, Tobias Henning, Nikolaus Marx, Joachim Jankowski, Heidi Noels. Platelet Function in CKD: A Systematic Review and Meta-Analysis. Journal of the American Society of Nephrology. 2021; 32 (7):1583-1598.

Chicago/Turabian Style

Constance C.F.M.J. Baaten; Marieke Sternkopf; Tobias Henning; Nikolaus Marx; Joachim Jankowski; Heidi Noels. 2021. "Platelet Function in CKD: A Systematic Review and Meta-Analysis." Journal of the American Society of Nephrology 32, no. 7: 1583-1598.

Editorial
Published: 09 December 2020 in Advanced Drug Delivery Reviews
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ACS Style

Twan Lammers; Heidi Noels. Lipids in disease pathology, diagnosis & therapy. Advanced Drug Delivery Reviews 2020, 159, 1 -3.

AMA Style

Twan Lammers, Heidi Noels. Lipids in disease pathology, diagnosis & therapy. Advanced Drug Delivery Reviews. 2020; 159 ():1-3.

Chicago/Turabian Style

Twan Lammers; Heidi Noels. 2020. "Lipids in disease pathology, diagnosis & therapy." Advanced Drug Delivery Reviews 159, no. : 1-3.

Review
Published: 06 November 2020 in Cells
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Cardiovascular calcification is highly prevalent and associated with increased morbidity in chronic kidney disease (CKD). This review examines the impact of uremic toxins, which accumulate in CKD due to a failing kidney function, on cardiovascular calcification. A systematic literature search identified 41 uremic toxins that have been studied in relation to cardiovascular calcification. For 29 substances, a potentially causal role in cardiovascular calcification was addressed in in vitro or animal studies. A calcification-inducing effect was revealed for 16 substances, whereas for three uremic toxins, namely the guanidino compounds asymmetric and symmetric dimethylarginine, as well as guanidinosuccinic acid, a calcification inhibitory effect was identified in vitro. At a mechanistic level, effects of uremic toxins on calcification could be linked to the induction of inflammation or oxidative stress, smooth muscle cell osteogenic transdifferentiation and/or apoptosis, or alkaline phosphatase activity. For all middle molecular weight and protein-bound uremic toxins that were found to affect cardiovascular calcification, an increasing effect on calcification was revealed, supporting the need to focus on an increased removal efficiency of these uremic toxin classes in dialysis. In conclusion, of all uremic toxins studied with respect to calcification regulatory effects to date, more uremic toxins promote rather than reduce cardiovascular calcification processes. Additionally, it highlights that only a relatively small part of uremic toxins has been screened for effects on calcification, supporting further investigation of uremic toxins, as well as of associated post-translational modifications, on cardiovascular calcification processes.

ACS Style

Jana Holmar; Sofia De La Puente-Secades; Jürgen Floege; Heidi Noels; Joachim Jankowski; Setareh Orth-Alampour. Uremic Toxins Affecting Cardiovascular Calcification: A Systematic Review. Cells 2020, 9, 2428 .

AMA Style

Jana Holmar, Sofia De La Puente-Secades, Jürgen Floege, Heidi Noels, Joachim Jankowski, Setareh Orth-Alampour. Uremic Toxins Affecting Cardiovascular Calcification: A Systematic Review. Cells. 2020; 9 (11):2428.

Chicago/Turabian Style

Jana Holmar; Sofia De La Puente-Secades; Jürgen Floege; Heidi Noels; Joachim Jankowski; Setareh Orth-Alampour. 2020. "Uremic Toxins Affecting Cardiovascular Calcification: A Systematic Review." Cells 9, no. 11: 2428.

Review article
Published: 27 July 2020 in Advanced Drug Delivery Reviews
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With cardiovascular disease being the leading cause of morbidity and mortality worldwide, effective and cost-efficient therapies to reduce cardiovascular risk are highly needed. Lipids and lipoprotein particles crucially contribute to atherosclerosis as underlying pathology of cardiovascular disease and influence inflammatory processes as well as function of leukocytes, vascular and cardiac cells, thereby impacting on vessels and heart. Statins form the first-line therapy with the aim to block cholesterol synthesis, but additional lipid-lowering drugs are sometimes needed to achieve low-density lipoprotein (LDL) cholesterol target values. Furthermore, beyond LDL cholesterol, also other lipid mediators contribute to cardiovascular risk. This review comprehensively discusses low- and high-density lipoprotein cholesterol, lipoprotein (a), triglycerides as well as fatty acids and derivatives in the context of cardiovascular disease, providing mechanistic insights into their role in pathological processes impacting on cardiovascular disease. Also, an overview of applied as well as emerging therapeutic strategies to reduce lipid-induced cardiovascular burden is provided.

ACS Style

Josefin Soppert; Michael Lehrke; Nikolaus Marx; Joachim Jankowski; Heidi Noels. Lipoproteins and lipids in cardiovascular disease: from mechanistic insights to therapeutic targeting. Advanced Drug Delivery Reviews 2020, 159, 4 -33.

AMA Style

Josefin Soppert, Michael Lehrke, Nikolaus Marx, Joachim Jankowski, Heidi Noels. Lipoproteins and lipids in cardiovascular disease: from mechanistic insights to therapeutic targeting. Advanced Drug Delivery Reviews. 2020; 159 ():4-33.

Chicago/Turabian Style

Josefin Soppert; Michael Lehrke; Nikolaus Marx; Joachim Jankowski; Heidi Noels. 2020. "Lipoproteins and lipids in cardiovascular disease: from mechanistic insights to therapeutic targeting." Advanced Drug Delivery Reviews 159, no. : 4-33.

Short communication
Published: 17 June 2020 in Biochemical and Biophysical Research Communications
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Vascular calcification (VC) is one major complication in patients with chronic kidney disease, with a misbalance in calcium and phosphate metabolism playing crucial role. The mechanisms underlying VC have not been entirely revealed to date. As studies aiming at the identification and characterization of the involved mediators are highly relevant, we developed a standardized operating protocol for in vitro and ex vivo approaches in this study to aiming at the comparability of these studies. We analyzed in vitro and ex vivo experimental conditions to study VC. Therefore, vascular smooth muscle cells were used for in vitro experiments and rat aorta for ex vivo experiments. The degree of calcification was estimated by quantification of calcium concentrations and by von Kossa staining. As a result, a step-by-step protocol for performing experiments on VC was established. We were able to demonstrate that the degree and the location of VC in vascular smooth muscle cells and aortic rings was highly dependent on the phosphate and CaCl2 concentration in the medium as well as the incubation time. Furthermore, the VC was reduced upon increasing fetal calf serum concentration in the medium. In the current study, we developed and validated a standardized operating protocol for systematic in vitro and ex vivo analyses of medial calcification, which is essential for the comparability of the results of future studies.

ACS Style

Jana Holmar; Heidi Noels; Michael Böhm; Shruti Bhargava; Joachim Jankowski; Setareh Orth-Alampour. Development, establishment and validation of in vitro and ex vivo assays of vascular calcification. Biochemical and Biophysical Research Communications 2020, 530, 462 -470.

AMA Style

Jana Holmar, Heidi Noels, Michael Böhm, Shruti Bhargava, Joachim Jankowski, Setareh Orth-Alampour. Development, establishment and validation of in vitro and ex vivo assays of vascular calcification. Biochemical and Biophysical Research Communications. 2020; 530 (2):462-470.

Chicago/Turabian Style

Jana Holmar; Heidi Noels; Michael Böhm; Shruti Bhargava; Joachim Jankowski; Setareh Orth-Alampour. 2020. "Development, establishment and validation of in vitro and ex vivo assays of vascular calcification." Biochemical and Biophysical Research Communications 530, no. 2: 462-470.

Editorial
Published: 11 June 2020 in Toxins
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With a mean worldwide prevalence of 13

ACS Style

Heidi Noels; Joachim Jankowski. Editorial on the Special Issue “Comorbidities in Chronic Kidney Disease”. Toxins 2020, 12, 1 .

AMA Style

Heidi Noels, Joachim Jankowski. Editorial on the Special Issue “Comorbidities in Chronic Kidney Disease”. Toxins. 2020; 12 (6):1.

Chicago/Turabian Style

Heidi Noels; Joachim Jankowski. 2020. "Editorial on the Special Issue “Comorbidities in Chronic Kidney Disease”." Toxins 12, no. 6: 1.

Journal article
Published: 01 January 2020 in Atherosclerosis
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IKKα is an important regulator of gene expression. As IKKα kinase inactivity in bone marrow-derived cells does not affect atherosclerosis, we here investigate the impact of a whole body-IKKα kinase inactivity on atherosclerosis. Apolipoprotein E (Apoe)-deficient mice homozygous for an activation-resistant Ikkα-mutant (IkkαAA/AAApoe-/-) and Ikkα+/+Apoe-/- controls received a Western-type diet. Atherosclerotic lesion size and cellular content were analyzed using histology and immunofluorescence. Vascular protein expression and IKKα kinase activity were quantified by Luminex multiplex immuno-assay and ELISA. A vascular site-specific IKKα expression and kinase activation profile was revealed, with higher total IKKα protein levels in aortic root but increased IKKα phosphorylation, representing activated IKKα, in the aortic arch. This was associated with a vascular site-specific effect of IkkαAA/AA knock-in on atherosclerosis: in the aortic root, IkkαAA/AA knock-in decreased lesion size by 22.0 ± 7.7% (p < 0.01), reduced absolute lesional smooth muscle cell numbers and lowered pro-atherogenic MMP2. In contrast, IkkαAA/AA knock-in increased lesion size in the aortic arch by 43.7 ± 20.1% (p < 0.001), increased the abundance of lesional smooth muscle cells in brachiocephalic artery as main arch side branch and elevated MMP2. A similar profile was observed for MMP3. No effects were observed on necrotic core or collagen deposition in atherosclerotic lesions, nor on absolute lesional macrophage numbers. A non-activatable IKKα kinase differentially affects atherosclerosis in aortic root vs. aortic arch/brachiocephalic artery, associated with a differential vascular IKKα expression and kinase activation profile as well as with a vascular site-dependent impact on lesional smooth muscle cell accumulation and protein expression profiles.

ACS Style

Pathricia V. Tilstam; Josefin Soppert; Christian Hemmers; Eva Harlacher; Yvonne Döring; Emiel P.C. van der Vorst; Corinna Schulte; Setareh Alampour-Rajabi; Wendy Theelen; Yaw Asare; Menno P.J. de Winther; Toby Lawrence; Jürgen Bernhagen; Andreas Schober; Alma Zernecke; Joachim Jankowski; Christian Weber; Heidi Noels. Non-activatable mutant of inhibitor of kappa B kinase α (IKKα) exerts vascular site-specific effects on atherosclerosis in Apoe-deficient mice. Atherosclerosis 2020, 292, 23 -30.

AMA Style

Pathricia V. Tilstam, Josefin Soppert, Christian Hemmers, Eva Harlacher, Yvonne Döring, Emiel P.C. van der Vorst, Corinna Schulte, Setareh Alampour-Rajabi, Wendy Theelen, Yaw Asare, Menno P.J. de Winther, Toby Lawrence, Jürgen Bernhagen, Andreas Schober, Alma Zernecke, Joachim Jankowski, Christian Weber, Heidi Noels. Non-activatable mutant of inhibitor of kappa B kinase α (IKKα) exerts vascular site-specific effects on atherosclerosis in Apoe-deficient mice. Atherosclerosis. 2020; 292 ():23-30.

Chicago/Turabian Style

Pathricia V. Tilstam; Josefin Soppert; Christian Hemmers; Eva Harlacher; Yvonne Döring; Emiel P.C. van der Vorst; Corinna Schulte; Setareh Alampour-Rajabi; Wendy Theelen; Yaw Asare; Menno P.J. de Winther; Toby Lawrence; Jürgen Bernhagen; Andreas Schober; Alma Zernecke; Joachim Jankowski; Christian Weber; Heidi Noels. 2020. "Non-activatable mutant of inhibitor of kappa B kinase α (IKKα) exerts vascular site-specific effects on atherosclerosis in Apoe-deficient mice." Atherosclerosis 292, no. : 23-30.

Journal article
Published: 03 July 2019 in Toxins
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Hydrophobic uremic toxins accumulate in patients with chronic kidney disease, contributing to a highly increased cardiovascular risk. The clearance of these uremic toxins using current hemodialysis techniques is limited due to their hydrophobicity and their high binding affinity to plasma proteins. Adsorber techniques may be an appropriate alternative to increase hydrophobic uremic toxin removal. We developed an extracorporeal, whole-blood bifunctional adsorber particle consisting of a porous, activated charcoal core with a hydrophilic polyvinylpyrrolidone surface coating. The adsorption capacity was quantified using analytical chromatography after perfusion of the particles with an albumin solution or blood, each containing mixtures of hydrophobic uremic toxins. A time-dependent increase in hydrophobic uremic toxin adsorption was depicted and all toxins showed a high binding affinity to the adsorber particles. Further, the particle showed a sufficient hemocompatibility without significant effects on complement component 5a, thrombin-antithrombin III complex, or thrombocyte concentration in blood in vitro, although leukocyte counts were slightly reduced. In conclusion, the bifunctional adsorber particle with cross-linked polyvinylpyrrolidone coating showed a high adsorption capacity without adverse effects on hemocompatibility in vitro. Thus, it may be an interesting candidate for further in vivo studies with the aim to increase the efficiency of conventional dialysis techniques.

ACS Style

Marieke Sternkopf; Sven Thoröe-Boveleth; Tobias Beck; Kirsten Oleschko; Ansgar Erlenkötter; Ulrich Tschulena; Sonja Steppan; Thimoteus Speer; Claudia Goettsch; Vera Jankowski; Joachim Jankowski; Heidi Noels; The European Uremic Toxin Work Group-EUTox. A Bifunctional Adsorber Particle for the Removal of Hydrophobic Uremic Toxins from Whole Blood of Renal Failure Patients. Toxins 2019, 11, 389 .

AMA Style

Marieke Sternkopf, Sven Thoröe-Boveleth, Tobias Beck, Kirsten Oleschko, Ansgar Erlenkötter, Ulrich Tschulena, Sonja Steppan, Thimoteus Speer, Claudia Goettsch, Vera Jankowski, Joachim Jankowski, Heidi Noels, The European Uremic Toxin Work Group-EUTox. A Bifunctional Adsorber Particle for the Removal of Hydrophobic Uremic Toxins from Whole Blood of Renal Failure Patients. Toxins. 2019; 11 (7):389.

Chicago/Turabian Style

Marieke Sternkopf; Sven Thoröe-Boveleth; Tobias Beck; Kirsten Oleschko; Ansgar Erlenkötter; Ulrich Tschulena; Sonja Steppan; Thimoteus Speer; Claudia Goettsch; Vera Jankowski; Joachim Jankowski; Heidi Noels; The European Uremic Toxin Work Group-EUTox. 2019. "A Bifunctional Adsorber Particle for the Removal of Hydrophobic Uremic Toxins from Whole Blood of Renal Failure Patients." Toxins 11, no. 7: 389.

Journal article
Published: 01 July 2019 in Atherosclerosis
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Members of the family of a disintegrin and metalloproteinases (ADAMs) and their substrates have been previously shown to modulate the inflammatory response in cardiac diseases, but studies investigating the relevance of ADAM8 are still rare. Our aim is to provide evidence for the inflammatory dysregulation of ADAM8 in vascular diseases and its association with disease severity. Western-type diet fed Apoe-/- and Ldlr-/- mice and artery ligation served as murine model for atherosclerosis and myocardial infarction, respectively. Human bypass grafts were used to study the association with coronary artery disease (CAD), with the simplified acute physiology score II (SAPS II) as a measure of postoperative organ dysfunction. Human primary vascular and blood cells were analyzed under basal and inflammatory conditions. mRNA levels were determined by RT-qPCR, ADAM8 protein levels by ELISA, immunohistochemistry or flow cytometry. ADAM8/ADAM8 expression is associated with atherosclerosis and CAD such as myocardial infarction in both mice and humans, especially in endothelial cells and leukocytes. We observed a strong in vivo and in vitro correlation of ADAM8 with the vascular disease markers VCAM-1, ICAM-1, TNF, IL-6, and CCL-2. Serum analysis revealed a significant elevation of soluble ADAM8 serum levels correlating with soluble CXCL16 levels and SAPS II. We demonstrate a general association of ADAM8 with cardiovascular diseases in mice and humans predominantly acting in endothelial cells and leukocytes. The correlation with postoperative organ dysfunctions in CAD patients highlights the value of further studies investigating the specific function of ADAM8 in cardiovascular diseases.

ACS Style

Daniel Schick; Aaron Babendreyer; Justyna Wozniak; Tanzeela Awan; Heidi Noels; Elisa A. Liehn; Jörg-W. Bartsch; Ann-Kathrin Vlacil; Karsten Grote; Rashad Zayat; Andreas Goetzenich; Andreas Ludwig; Daniela Dreymueller. Elevated expression of the metalloproteinase ADAM8 associates with vascular diseases in mice and humans. Atherosclerosis 2019, 286, 163 -171.

AMA Style

Daniel Schick, Aaron Babendreyer, Justyna Wozniak, Tanzeela Awan, Heidi Noels, Elisa A. Liehn, Jörg-W. Bartsch, Ann-Kathrin Vlacil, Karsten Grote, Rashad Zayat, Andreas Goetzenich, Andreas Ludwig, Daniela Dreymueller. Elevated expression of the metalloproteinase ADAM8 associates with vascular diseases in mice and humans. Atherosclerosis. 2019; 286 ():163-171.

Chicago/Turabian Style

Daniel Schick; Aaron Babendreyer; Justyna Wozniak; Tanzeela Awan; Heidi Noels; Elisa A. Liehn; Jörg-W. Bartsch; Ann-Kathrin Vlacil; Karsten Grote; Rashad Zayat; Andreas Goetzenich; Andreas Ludwig; Daniela Dreymueller. 2019. "Elevated expression of the metalloproteinase ADAM8 associates with vascular diseases in mice and humans." Atherosclerosis 286, no. : 163-171.

Journal article
Published: 10 October 2018 in Neurology
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Objective To isolate and identify a new, as yet unknown molecule in CSF that could serve as marker for Alzheimer disease. Methods We immunized mice with human CSF and fused hybridomas for monoclonal antibodies and screened these antibodies for their capacity to discriminate CSF of patients with Alzheimer disease from CSF of controls. We then chromatographically isolated the antigen to the best discriminating antibody and identified the antigen using mass spectrometric methods. Thereafter, we quantified the CSF concentration of the antigen in a new cohort of patients with Alzheimer disease and controls and performed immunohistochemistry of postmortem brain tissue derived from patients with Alzheimer disease and controls. Results We generated >200 hybridomas and selected 1 antibody that discriminated CSF from patients with Alzheimer disease from that of controls. We identified golgin A4 as the antigen detected by this antibody. Golgin A4 concentration was significantly higher in CSF from patients with Alzheimer disease than in CSF of controls (145 [interquartile range 125–155] vs 115 [ 99–128] pg/mL, p < 0.001) and demonstrated a substantial discriminative power (area under the receiver operating characteristic curve 0.80, 95% confidence interval 0.67–0.94). Immunohistochemistry of postmortem brain sections from patients with Alzheimer disease revealed a significant accumulation of golgin A4 in granulovacuolar degeneration bodies (GVBs). Conclusions These results support the notion that golgin A4 could serve as a diagnostic marker in Alzheimer disease. For validation of this notion, prospective multicenter diagnostic studies will evaluate golgin A4 as diagnostic marker for Alzheimer disease. Furthermore, it has to be determined whether the association of golgin A4 with GVBs is an epiphenomenon or whether golgin A4 plays a more direct role in Alzheimer disease, allowing it to serve as a target in therapeutic treatment strategies. Classification of evidence This study provides Class III evidence that elevated CSF golgin A4 levels identify patients with Alzheimer disease.

ACS Style

Felix Kork; Joachim Jankowski; Anand Goswami; Joachim Weis; Gary Brook; Alfred Yamoah; Jasper Anink; Eleonora Aronica; Stefan Fritz; Carmen Huck; Carola Schipke; Oliver Peters; Martin Tepel; Heidi Noels; Vera Jankowski. Golgin A4 in CSF and granulovacuolar degenerations of patients with Alzheimer disease. Neurology 2018, 91, e1799 -e1808.

AMA Style

Felix Kork, Joachim Jankowski, Anand Goswami, Joachim Weis, Gary Brook, Alfred Yamoah, Jasper Anink, Eleonora Aronica, Stefan Fritz, Carmen Huck, Carola Schipke, Oliver Peters, Martin Tepel, Heidi Noels, Vera Jankowski. Golgin A4 in CSF and granulovacuolar degenerations of patients with Alzheimer disease. Neurology. 2018; 91 (19):e1799-e1808.

Chicago/Turabian Style

Felix Kork; Joachim Jankowski; Anand Goswami; Joachim Weis; Gary Brook; Alfred Yamoah; Jasper Anink; Eleonora Aronica; Stefan Fritz; Carmen Huck; Carola Schipke; Oliver Peters; Martin Tepel; Heidi Noels; Vera Jankowski. 2018. "Golgin A4 in CSF and granulovacuolar degenerations of patients with Alzheimer disease." Neurology 91, no. 19: e1799-e1808.

Observational study
Published: 07 August 2018 in Scientific Reports
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Cardiac surgery with cardiopulmonary bypass (CPB) triggers myocardial ischemia/reperfusion injury contributing to organ dysfunction. Preclinical studies revealed that dipeptidyl peptidase (DPP4) inhibition is protective during myocardial infarction. Here, we assessed for the first time the relation of peri-operative DPP4-activity in serum of 46 patients undergoing cardiac surgery with patients' post-operative organ dysfunction during intensive care unit (ICU) stay. Whereas a prior myocardial infarction significantly reduced pre-operative DDP4-activity, patients with preserved left ventricular function showed an intra-operative decrease of DPP4-activity. The latter correlated with aortic cross clamping time, indicative for the duration of surgery-induced myocardial ischemia. As underlying mechanism, mass-spectrometry revealed increased DPP4 oxidation by cardiac surgery, with DPP4 oxidation reducing DPP4-activity in vitro. Further, post-operative DPP4-activity was negatively correlated with the extent of post-operative organ injury as measured by SAPS II and SOFA scoring, circulating levels of creatinine and lactate, as well as patients' stay on the ICU. In conclusion, cardiac surgery reduces DPP4-activity through oxidation, with low post-operative DPP4-activity being associated with organ dysfunction and worse outcome of patients during the post-operative ICU stay. This likely reflects the severity of myocardial ischemia/reperfusion injury and may suggest potential beneficial effects of anti-oxidative treatments during cardiac surgery.

ACS Style

Heidi Noels; Wendy Theelen; Marieke Sternkopf; Vera Jankowski; Julia Moellmann; Sandra Kraemer; Michael Lehrke; Nikolaus Marx; Lukas Martin; Gernot Marx; Joachim Jankowski; Andreas Goetzenich; Christian Stoppe. Reduced post-operative DPP4 activity associated with worse patient outcome after cardiac surgery. Scientific Reports 2018, 8, 11820 .

AMA Style

Heidi Noels, Wendy Theelen, Marieke Sternkopf, Vera Jankowski, Julia Moellmann, Sandra Kraemer, Michael Lehrke, Nikolaus Marx, Lukas Martin, Gernot Marx, Joachim Jankowski, Andreas Goetzenich, Christian Stoppe. Reduced post-operative DPP4 activity associated with worse patient outcome after cardiac surgery. Scientific Reports. 2018; 8 (1):11820.

Chicago/Turabian Style

Heidi Noels; Wendy Theelen; Marieke Sternkopf; Vera Jankowski; Julia Moellmann; Sandra Kraemer; Michael Lehrke; Nikolaus Marx; Lukas Martin; Gernot Marx; Joachim Jankowski; Andreas Goetzenich; Christian Stoppe. 2018. "Reduced post-operative DPP4 activity associated with worse patient outcome after cardiac surgery." Scientific Reports 8, no. 1: 11820.

Journal article
Published: 12 July 2018 in Scientific Reports
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Macrophage-derived foam cells are key regulators of atherogenesis. They accumulate in atherosclerotic plaques and support inflammatory processes by producing cytokines and chemokines. Identifying factors that regulate macrophage lipid uptake may reveal therapeutic targets for coronary artery disease (CAD). Here, we establish a high-throughput screening workflow to systematically identify genes that impact the uptake of DiI-labeled low-density lipoprotein (LDL) into monocyte-derived primary human macrophages. For this, monocytes isolated from peripheral blood were seeded onto 384-well plates, solid-phase transfected with siRNAs, differentiated in vitro into macrophages, and LDL-uptake per cell was measured by automated microscopy and quantitative image analysis. We applied this workflow to study how silencing of 89 genes impacts LDL-uptake into cells from 16 patients with CAD and 16 age-matched controls. Silencing of four novel genes (APOC1, CMTM6, FABP4, WBP5) reduced macrophage LDL-uptake. Additionally, knockdown of the chemokine receptor CXCR4 reduced LDL-uptake, most likely through a G-protein coupled mechanism that involves the CXCR4 ligand macrophage-induced factor (MIF), but is independent of CXCL12. We introduce a high-throughput strategy to systematically study gene function directly in primary CAD-patient cells. Our results propose a function for the MIF/CXCR4 signaling pathway, as well as several novel candidate genes impacting lipid uptake into human macrophages.

ACS Style

Gabriele Domschke; Fabian Linden; Lukas Pawig; Anna Hafner; Mohammadreza Akhavanpoor; Jürgen Reymann; Andreas O. Doesch; Christian Erbel; Christian Weber; Hugo A. Katus; Heidi Noels; Holger Erfle; Christian A. Gleissner; Heiko Runz. Systematic RNA-interference in primary human monocyte-derived macrophages: A high-throughput platform to study foam cell formation. Scientific Reports 2018, 8, 10516 .

AMA Style

Gabriele Domschke, Fabian Linden, Lukas Pawig, Anna Hafner, Mohammadreza Akhavanpoor, Jürgen Reymann, Andreas O. Doesch, Christian Erbel, Christian Weber, Hugo A. Katus, Heidi Noels, Holger Erfle, Christian A. Gleissner, Heiko Runz. Systematic RNA-interference in primary human monocyte-derived macrophages: A high-throughput platform to study foam cell formation. Scientific Reports. 2018; 8 (1):10516.

Chicago/Turabian Style

Gabriele Domschke; Fabian Linden; Lukas Pawig; Anna Hafner; Mohammadreza Akhavanpoor; Jürgen Reymann; Andreas O. Doesch; Christian Erbel; Christian Weber; Hugo A. Katus; Heidi Noels; Holger Erfle; Christian A. Gleissner; Heiko Runz. 2018. "Systematic RNA-interference in primary human monocyte-derived macrophages: A high-throughput platform to study foam cell formation." Scientific Reports 8, no. 1: 10516.

Conference paper
Published: 30 May 2018 in VI Latin American Congress on Biomedical Engineering CLAIB 2014, Paraná, Argentina 29, 30 & 31 October 2014
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Approximately 8–10% of the adult population in Europe suffers from kidney diseases. Cardiovascular complications are the leading cause of death in chronic kidney disease (CKD) patients, and vascular calcification is prevalent. High serum phosphate (P) level is a trigger of higher prevalence of vascular calcification in CKD patients. Phosphate is removed from the blood of end-stage renal disease (ESRD) patients regularly by extracorporeal renal replacement therapy, called dialysis. This paper aims to evaluate the calcification capability of CKD phosphate levels and compare the removal of phosphate during the different dialysis modalities. Human vascular smooth muscle cells and rat aortic rings were incubated in a medium containing CKD levels of phosphate. Both, calcium content measurements and histochemical staining proofed significantly increased calcification. Ten uremic patients, five males, and five females mean age 59 ± 16 years, were followed during 40 chronic midweek hemodialysis sessions. Four dialysis modalities with different settings were used once for each patient: hemodialysis (HD), high-flux hemodialysis (HF1, HF2) and postdilutional online hemodiafiltration (HDF). Total removed phosphate (TRP) was calculated by using phosphate concentration and the weight of the total spent dialysate collection. Phosphate reduction ratio (RR) was calculated by using patients’ pre- and post-dialysis phosphate concentrations in serum. Patients’ mean pre-dialysis serum phosphate levels were 1.72 ± 0.57 mmol/L, which is higher than in healthy subjects (0.81–1.45 mmol/L). Phosphate serum reduction ratios achieved during HD procedures were significantly lower from the ratios achieved during HDF and HF2 procedures. The mean total removed phosphate (TRP) values for HD were significantly lower than TRP values of other modalities (HF1, HF2, and HDF). Differences in removal values between HF1, HF2, and HDF were not significant. The results are indicating that phosphate levels presented in CKD increase vascular calcification and it is possible to remove phosphate more effectively by adjusting the dialysis treatment parameters.

ACS Style

Jana Holmar; Ivo Fridolin; Merike Luman; Joachim Jankowski; Heidi Noels; Vera Jankowski; Setareh Alampour-Rajabi. Removal of Vascular Calcification Inducer Phosphate in Different Dialysis Treatment Modalities. VI Latin American Congress on Biomedical Engineering CLAIB 2014, Paraná, Argentina 29, 30 & 31 October 2014 2018, 143 -147.

AMA Style

Jana Holmar, Ivo Fridolin, Merike Luman, Joachim Jankowski, Heidi Noels, Vera Jankowski, Setareh Alampour-Rajabi. Removal of Vascular Calcification Inducer Phosphate in Different Dialysis Treatment Modalities. VI Latin American Congress on Biomedical Engineering CLAIB 2014, Paraná, Argentina 29, 30 & 31 October 2014. 2018; ():143-147.

Chicago/Turabian Style

Jana Holmar; Ivo Fridolin; Merike Luman; Joachim Jankowski; Heidi Noels; Vera Jankowski; Setareh Alampour-Rajabi. 2018. "Removal of Vascular Calcification Inducer Phosphate in Different Dialysis Treatment Modalities." VI Latin American Congress on Biomedical Engineering CLAIB 2014, Paraná, Argentina 29, 30 & 31 October 2014 , no. : 143-147.

Journal article
Published: 22 May 2018 in Acta Physiologica
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Corinna Schulte; Heidi Noels. Interferon-induced protein 35 inhibits endothelial cell proliferation, migration and re-endothelialization of injured arteries by inhibiting the nuclear factor-kappa B pathway. Acta Physiologica 2018, 223, e13091 .

AMA Style

Corinna Schulte, Heidi Noels. Interferon-induced protein 35 inhibits endothelial cell proliferation, migration and re-endothelialization of injured arteries by inhibiting the nuclear factor-kappa B pathway. Acta Physiologica. 2018; 223 (3):e13091.

Chicago/Turabian Style

Corinna Schulte; Heidi Noels. 2018. "Interferon-induced protein 35 inhibits endothelial cell proliferation, migration and re-endothelialization of injured arteries by inhibiting the nuclear factor-kappa B pathway." Acta Physiologica 223, no. 3: e13091.

Review
Published: 04 May 2018 in Clinical Research in Cardiology
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Patients with chronic kidney disease (CKD) exhibit a massively increased risk for cardiovascular (CV) events, and traditional strategies to improve CV outcome have largely failed in the context of CKD. This review article summarizes the current understanding of the pathophysiology of CVD in patients with CKD, defines the gaps in knowledge and describes the structure of the German Transregional Research Consortium SFB TRR219 which addresses “Mechanisms of Cardiovascular Complications in Chronic Kidney Disease”.

ACS Style

Nikolaus Marx; Heidi Noels; Joachim Jankowski; Jürgen Floege; Danilo Fliser; Michael Böhm. Mechanisms of cardiovascular complications in chronic kidney disease: research focus of the Transregional Research Consortium SFB TRR219 of the University Hospital Aachen (RWTH) and the Saarland University. Clinical Research in Cardiology 2018, 107, 120 -126.

AMA Style

Nikolaus Marx, Heidi Noels, Joachim Jankowski, Jürgen Floege, Danilo Fliser, Michael Böhm. Mechanisms of cardiovascular complications in chronic kidney disease: research focus of the Transregional Research Consortium SFB TRR219 of the University Hospital Aachen (RWTH) and the Saarland University. Clinical Research in Cardiology. 2018; 107 (2):120-126.

Chicago/Turabian Style

Nikolaus Marx; Heidi Noels; Joachim Jankowski; Jürgen Floege; Danilo Fliser; Michael Böhm. 2018. "Mechanisms of cardiovascular complications in chronic kidney disease: research focus of the Transregional Research Consortium SFB TRR219 of the University Hospital Aachen (RWTH) and the Saarland University." Clinical Research in Cardiology 107, no. 2: 120-126.

Journal article
Published: 01 May 2018 in Nephrology Dialysis Transplantation
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INTRODUCTION AND AIMS: Patients with chronic kidney disease (CKD) have an increased risk of cardiovascular disease. This includes a high risk for atherosclerosis-related complications such as ischemic heart disease, and mouse models have shown that CKD increases atherosclerosis. The CXCL12/CXCR4 chemokine ligand/receptor axis controls cell homeostasis. So far, an atheroprotective role of CXCL12/CXCR4 has only been implied through pharmacological intervention, and cell-specific effects of CXCR4 in the arterial wall remain elusive. This prompted us to investigate the relevance of vascular CXCR4 in atherosclerosis.

ACS Style

Heidi Noels; Yvonne Döring; Emiel Van Der Vorst; Virginia Egea; Maik Drechsler; Katrin Schröder; Remco Megens; Barbara Klinkhammer; Peter Boor; Leon Schurgers; Rick Van Gorp; Christian Ries; Pascal Kusters; Allard Van Der Wal; Tilman Hackeng; Gabor Gäbel; Ralf Brandes; Oliver Soehnlein; Esther Lutgens; Dietmar Vestweber; Daniel Teupser; Lesca Holdt; Daniel Rader; Danish Saleheen; Christian Weber. FP526VASCULAR CXCR4 LIMITS ATHEROSCLEROSIS BY MAINTAINING ARTERIAL INTEGRITY. Nephrology Dialysis Transplantation 2018, 33, i216 -i216.

AMA Style

Heidi Noels, Yvonne Döring, Emiel Van Der Vorst, Virginia Egea, Maik Drechsler, Katrin Schröder, Remco Megens, Barbara Klinkhammer, Peter Boor, Leon Schurgers, Rick Van Gorp, Christian Ries, Pascal Kusters, Allard Van Der Wal, Tilman Hackeng, Gabor Gäbel, Ralf Brandes, Oliver Soehnlein, Esther Lutgens, Dietmar Vestweber, Daniel Teupser, Lesca Holdt, Daniel Rader, Danish Saleheen, Christian Weber. FP526VASCULAR CXCR4 LIMITS ATHEROSCLEROSIS BY MAINTAINING ARTERIAL INTEGRITY. Nephrology Dialysis Transplantation. 2018; 33 (suppl_1):i216-i216.

Chicago/Turabian Style

Heidi Noels; Yvonne Döring; Emiel Van Der Vorst; Virginia Egea; Maik Drechsler; Katrin Schröder; Remco Megens; Barbara Klinkhammer; Peter Boor; Leon Schurgers; Rick Van Gorp; Christian Ries; Pascal Kusters; Allard Van Der Wal; Tilman Hackeng; Gabor Gäbel; Ralf Brandes; Oliver Soehnlein; Esther Lutgens; Dietmar Vestweber; Daniel Teupser; Lesca Holdt; Daniel Rader; Danish Saleheen; Christian Weber. 2018. "FP526VASCULAR CXCR4 LIMITS ATHEROSCLEROSIS BY MAINTAINING ARTERIAL INTEGRITY." Nephrology Dialysis Transplantation 33, no. suppl_1: i216-i216.

Journal article
Published: 01 May 2018 in Nephrology Dialysis Transplantation
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INTRODUCTION AND AIMS: Since post-translational modifications of proteins may have an impact on the pathogenesis of diseases like atherosclerosis, diabetes mellitus and chronic kidney disease (CKD), post-translational modifications are currently gaining increasing interest. In this study, a comprehensive method for analysis of these post-translational modifications is established for the clinical diagnostic routine.

ACS Style

Joachim Jankowski; Vera Jankowski; Heidi Noels. FP298POST-TRANSLATIONAL MODIFICATION OF PLASMA PROTEINS DECREASED BINDING CAPACITY FOR HYDROPHOBIC METABOLITES. Nephrology Dialysis Transplantation 2018, 33, i132 -i132.

AMA Style

Joachim Jankowski, Vera Jankowski, Heidi Noels. FP298POST-TRANSLATIONAL MODIFICATION OF PLASMA PROTEINS DECREASED BINDING CAPACITY FOR HYDROPHOBIC METABOLITES. Nephrology Dialysis Transplantation. 2018; 33 (suppl_1):i132-i132.

Chicago/Turabian Style

Joachim Jankowski; Vera Jankowski; Heidi Noels. 2018. "FP298POST-TRANSLATIONAL MODIFICATION OF PLASMA PROTEINS DECREASED BINDING CAPACITY FOR HYDROPHOBIC METABOLITES." Nephrology Dialysis Transplantation 33, no. suppl_1: i132-i132.

Journal article
Published: 01 May 2018 in Nephrology Dialysis Transplantation
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INTRODUCTION AND AIMS: Regardless of extensive studies, the molecular basis of hypertension is not well established, which makes it difficult to identify the best approach to lower blood pressure. We, therefore, performed plasma proteomics of plasma from patients with hypertension to identify molecular determinants detectable in these subjects but not in controls and vice versa.

ACS Style

Shruti Bhargava; Vera Jankowski; Heidi Noels; Pratibha Gajalla; Joachim Jankowski. SP080IDENTIFICATION OF MOLECULAR SIGNATURES IN HYPERSENSITIVE PATIENTS. Nephrology Dialysis Transplantation 2018, 33, i372 -i373.

AMA Style

Shruti Bhargava, Vera Jankowski, Heidi Noels, Pratibha Gajalla, Joachim Jankowski. SP080IDENTIFICATION OF MOLECULAR SIGNATURES IN HYPERSENSITIVE PATIENTS. Nephrology Dialysis Transplantation. 2018; 33 (suppl_1):i372-i373.

Chicago/Turabian Style

Shruti Bhargava; Vera Jankowski; Heidi Noels; Pratibha Gajalla; Joachim Jankowski. 2018. "SP080IDENTIFICATION OF MOLECULAR SIGNATURES IN HYPERSENSITIVE PATIENTS." Nephrology Dialysis Transplantation 33, no. suppl_1: i372-i373.

Journal article
Published: 01 May 2018 in Nephrology Dialysis Transplantation
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INTRODUCTION AND AIMS: The octapeptide angiotensin II (Ang II) is essential in the physiology and pathology of vascular regulation. Ang II is the principal vasoactive substance of the renin-angiotensin system (RAS), having a variety of physiological actions. In the past few years, the classical concept of the renin-angiotensin system (RAS) has experienced substantial conceptual changes. Angiotensin peptides such as Ang 1-7, Ang III and Ang IV were identified as mediators involved in vascular regulation. Here, we describe two novel Ang II-related substances in plasma from healthy humans and end-stage renal failure patients.

ACS Style

Setareh Orth-Alampour; Corinna Schmitz; Joachim Jankowski; Walter Zidek; Heidi Noels; Vera Jankowski. FP561IDENTIFICATION OF ANGIOTENSIN PEPTIDES MODULATING THE HARMFUL EFFECTS OF ANG II IN CHRONIC RENAL FAILURE. Nephrology Dialysis Transplantation 2018, 33, i229 -i229.

AMA Style

Setareh Orth-Alampour, Corinna Schmitz, Joachim Jankowski, Walter Zidek, Heidi Noels, Vera Jankowski. FP561IDENTIFICATION OF ANGIOTENSIN PEPTIDES MODULATING THE HARMFUL EFFECTS OF ANG II IN CHRONIC RENAL FAILURE. Nephrology Dialysis Transplantation. 2018; 33 (suppl_1):i229-i229.

Chicago/Turabian Style

Setareh Orth-Alampour; Corinna Schmitz; Joachim Jankowski; Walter Zidek; Heidi Noels; Vera Jankowski. 2018. "FP561IDENTIFICATION OF ANGIOTENSIN PEPTIDES MODULATING THE HARMFUL EFFECTS OF ANG II IN CHRONIC RENAL FAILURE." Nephrology Dialysis Transplantation 33, no. suppl_1: i229-i229.