Sajoscha Sorrentino

Publications

• 12.54

  Impact points

  Nebivolol exerts beneficial effects on endothelial function, early endothelial progenitor cells, myocardial neovascularization, and left ventricular dysfunction early after myocardial infarction beyond conventional β1-blockade.

  Sajoscha A Sorrentino, Carola Doerries, Costantina Manes, Thimoteus Speer, Chantal Dessy, Irina Lobysheva, Wazma Mohmand, Razma Akbar, Ferdinand Bahlmann, Christian Besler, Arnd Schaefer, Denise Hilfiker-Kleiner, Thomas F Lüscher, Jean-Luc Balligand, Helmut Drexler, Ulf Landmesser

  Journal of the American College of Cardiology. 02/2011; 57(5):601-11.

  The aim of this study was to investigate whether nebivolol has added effects on left ventricular (LV) dysfunction and remodeling early after myocardial infarction (MI) beyond its β₁-receptor-blocking properties. Nebivolol is a third-generation selective β₁-adrenoreceptor antagonist that stimulates e... [more] The aim of this study was to investigate whether nebivolol has added effects on left ventricular (LV) dysfunction and remodeling early after myocardial infarction (MI) beyond its β₁-receptor-blocking properties. Nebivolol is a third-generation selective β₁-adrenoreceptor antagonist that stimulates endothelial cell nitric oxide (NO) production and prevents vascular reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation. Both endothelial NO synthase-derived NO production and NADPH oxidase activation are critical modulators of LV dysfunction early after MI. Mice with extensive anterior MI (n = 90) were randomized to treatment with nebivolol (10 mg/kg/day), metoprolol-succinate (20 mg/kg/day), or placebo for 30 days starting on day 1 after surgery. Infarct size was similar among the groups. Both β₁-adrenergic receptor antagonists caused a similar decrease in heart rate. Nebivolol therapy improved endothelium-dependent vasorelaxation and increased early endothelial progenitor cells 4 weeks after MI compared with metoprolol and placebo. Nebivolol, but not metoprolol, inhibited cardiac NADPH oxidase activation after MI, as detected by electron spin resonance spectroscopy analysis. Importantly, nebivolol, but not metoprolol, improved LV dysfunction 4 weeks after MI (LV ejection fraction: nebivolol vs. metoprolol vs. placebo: 32 ± 4% vs. 17 ± 6% vs. 19 ± 4%; nebivolol vs. metoprolol: p < 0.05) and was associated with improved survival 4 weeks post-MI compared with placebo. Nebivolol had a significantly more pronounced inhibitory effect on cardiomyocyte hypertrophy after MI compared with metoprolol. Nebivolol improves LV dysfunction and survival early after MI likely beyond the effects provided by conventional β₁-receptor blockade. Nebivolol induced effects on NO-mediated endothelial function, early endothelial progenitor cells and inhibition of myocardial NADPH oxidase likely contribute to these beneficial effects of nebivolol early after MI.
• 6.37

  Impact points

  High permeability dialysis membrane allows effective removal of myoglobin in acute kidney injury resulting from rhabdomyolysis.

  Sajoscha A Sorrentino, Jan T Kielstein, Alexander Lukasz, Janine-Nicole Sorrentino, Bernhard Gohrbandt, Hermann Haller, Bernhard M W Schmidt

  Critical care medicine. 11/2010; 39(1):184-6.

  The objective of this study was to test the ability of myoglobin removal of a novel, high-permeability polysulphone dialyzer in acute kidney injury as a result of rhabdomyolysis. Intensive care unit of a tertiary care hospital. Six patients (one female; aged 24, 36, 41, 55, 63, and 65 yrs) with olig... [more] The objective of this study was to test the ability of myoglobin removal of a novel, high-permeability polysulphone dialyzer in acute kidney injury as a result of rhabdomyolysis. Intensive care unit of a tertiary care hospital. Six patients (one female; aged 24, 36, 41, 55, 63, and 65 yrs) with oligoanuric acute kidney injury resulting from rhabdomyolysis. Extended dialysis was performed using a single-pass batch dialysis system and a novel polysulphone high-flux dialyzer (effective surface area 1.8 m; inner lumen 220 μm; wall thickness 35 μm; allowing elimination of substances with a molecular weight of up to 30 kDa). Samples were collected at prefilter and postfilter sites as well as from the collected spent dialysate. The dialyzer clearance was calculated from concentrations before and directly after the dialysis membrane, the blood flow, and the ultrafiltration rate. The total amount of the myoglobin removed was measured directly as the whole dialysate was preserved. A median myoglobin clearance of 90.5 mL/min (range, 52.4-126.3 mL/min) was achieved, resulting in a median myoglobin removal per treatment hour of 0.54 g (range, 0.15-2.21 g). Extended dialysis with a high-flux, high-permeability membrane allowed effective elimination of myoglobin with a clearance of myoglobin that surpassed all previously reported dialysis techniques. This membrane may be advantageous in preventing acute kidney injury or avoiding complete loss of kidney function in patients with rhabdomyolysis. Further studies are needed to determine whether improving renal recovery or mortality in patients with acute kidney injury resulting from rhabdomyolysis is possible.
• 7.19

  Impact points

  Impaired endothelial repair capacity of early endothelial progenitor cells in prehypertension: relation to endothelial dysfunction.

  Giovanna Giannotti, Carola Doerries, Pavani S Mocharla, Maja F Mueller, Ferdinand H Bahlmann, Tibor Horvàth, Hong Jiang, Sajoscha A Sorrentino, Nora Steenken, Costantina Manes, Mario Marzilli, K Lenhard Rudolph, Thomas F Lüscher, Helmut Drexler, Ulf Landmesser

  Hypertension. 06/2010; 55(6):1389-97.

  Prehypertension is a highly frequent condition associated with an increased cardiovascular risk. Endothelial dysfunction is thought to promote the development of hypertension and vascular disease; however, underlying mechanisms remain to be further determined. The present study characterizes for the... [more] Prehypertension is a highly frequent condition associated with an increased cardiovascular risk. Endothelial dysfunction is thought to promote the development of hypertension and vascular disease; however, underlying mechanisms remain to be further determined. The present study characterizes for the first time the in vivo endothelial repair capacity of early endothelial progenitor cells (EPCs) in patients with prehypertension/hypertension and examines its relation with endothelial function. Early EPCs were isolated from healthy subjects and newly diagnosed prehypertensive and hypertensive patients (n=52). In vivo endothelial repair capacity of EPCs was examined by transplantation into a nude mouse carotid injury model. EPC senescence was determined (RT-PCR of telomere length). NO and superoxide production of EPCs were measured using electron spin resonance spectroscopy analysis. CD34(+)/KDR(+) mononuclear cells and circulating endothelial microparticles were examined by fluorescence-activated cell sorter analysis. Endothelium-dependent and -independent vasodilations were determined by high-resolution ultrasound. In vivo endothelial repair capacity of EPCs was substantially impaired in prehypertensive/hypertensive patients as compared with healthy subjects (re-endothelialized area: 15+/-3%/13+/-2% versus 28+/-3%; P<0.05 versus healthy subjects). Senescence of EPCs in prehypertension/hypertension was substantially increased, and NO production was markedly reduced. Moreover, reduced endothelial repair capacity of early EPCs was significantly related to an accelerated senescence of early EPCs and impaired endothelial function. The present study demonstrates for the first time that in vivo endothelial repair capacity of early EPCs is reduced in patients with prehypertension and hypertension, is related to EPC senescence and impaired endothelial function, and likely represents an early event in the development of hypertension.
• 0.47

  Impact points

  [Allopurinol-induced hypersensitivity syndrome resulting in death].

  Sören Laurisch, Maren Jaedtke, Reyhan Demir, Sajoscha A Sorrentino, Jan T Kielstein, Hans-Oliver Rennekampff, Peter M Vogt, Gerd P Meyer, Martin Fuchs, Gunnar Klein, Hartmut Drexler, Bernhard Schieffer, L Christian Napp

  Medizinische Klinik (Munich, Germany : 1983). 04/2010; 105(4):262-6.

  The present report describes the case of a 67-year-old patient who developed an allopurinol-induced hypersensitivity syndrome (AHS) with toxic epidermal necrolysis and subsequently died of septic multiorgan failure. Considering the increasing prescription rate of allopurinol, the present case report... [more] The present report describes the case of a 67-year-old patient who developed an allopurinol-induced hypersensitivity syndrome (AHS) with toxic epidermal necrolysis and subsequently died of septic multiorgan failure. Considering the increasing prescription rate of allopurinol, the present case report intends to demonstrate the underestimated threat of AHS.
• 14.82

  Impact points

  Endothelial-Vasoprotective Effects of High-Density Lipoprotein Are Impaired in Patients With Type 2 Diabetes Mellitus but Are Improved After Extended-Release Niacin Therapy.

  Sajoscha A Sorrentino, Christian Besler, Lucia Rohrer, Martin Meyer, Kathrin Heinrich, Ferdinand H Bahlmann, Maja Mueller, Tibor Horváth, Carola Doerries, Mariko Heinemann, Stella Flemmer, Andrea Markowski, Costantina Manes, Matthias J Bahr, Hermann Haller, Arnold von Eckardstein, Helmut Drexler, Ulf Landmesser

  Circulation. 12/2009;

  BACKGROUND: -High-density lipoprotein (HDL)-raising therapies are currently under intense evaluation, but the effects of HDL may be highly heterogeneous. We therefore compared the endothelial effects of HDL from healthy subjects and from patients with type 2 diabetes mellitus and low HDL (meeting th... [more] BACKGROUND: -High-density lipoprotein (HDL)-raising therapies are currently under intense evaluation, but the effects of HDL may be highly heterogeneous. We therefore compared the endothelial effects of HDL from healthy subjects and from patients with type 2 diabetes mellitus and low HDL (meeting the criteria for metabolic syndrome), who are frequently considered for HDL-raising therapies. Moreover, in diabetic patients, we examined the impact of extended-release (ER) niacin therapy on the endothelial effects of HDL. Methods and Results-HDL was isolated from healthy subjects (n=10) and patients with type 2 diabetes (n=33) by sequential ultracentrifugation. Effects of HDL on endothelial nitric oxide and superoxide production were characterized by electron spin resonance spectroscopy analysis. Effects of HDL on endothelium-dependent vasodilation and early endothelial progenitor cell-mediated endothelial repair were examined. Patients with diabetes were randomized to a 3-month therapy with ER niacin (1500 mg/d) or placebo, and endothelial effects of HDL were characterized. HDL from healthy subjects stimulated endothelial nitric oxide production, reduced endothelial oxidant stress, and improved endothelium-dependent vasodilation and early endothelial progenitor cell-mediated endothelial repair. In contrast, these beneficial endothelial effects of HDL were not observed in HDL from diabetic patients, which suggests markedly impaired endothelial-protective properties of HDL. ER niacin therapy improved the capacity of HDL to stimulate endothelial nitric oxide, to reduce superoxide production, and to promote endothelial progenitor cell-mediated endothelial repair. Further measurements suggested increased lipid oxidation of HDL in diabetic patients, and a reduction after ER niacin therapy. Conclusions-HDL from patients with type 2 diabetes mellitus and metabolic syndrome has substantially impaired endothelial-protective effects compared with HDL from healthy subjects. ER niacin therapy not only increases HDL plasma levels but markedly improves endothelial-protective functions of HDL in these patients, which is potentially more important. Clinical Trial Registration-clinicaltrials.gov. Identifier: NCT00346970.
• 4.64

  Impact points

  A Novel Small Animal Model for Accelerated Investigation of Tissue Engineered Aortic Valved Conduits.

  Klaus Kallenbach, Sajoscha Sorrentino, Heike Mertsching, Sawa Kostin, Klaus Pethig, Axel Haverich Md, Serghei Cebotari

  Tissue engineering. Part C, Methods. 05/2009;

  Objective: To describe a novel small animal model of tissue engineered aortic valved conduits aimed to investigate biological processes in an accelerated and inexpensive fashion. Methods: An isogenic Lewis to Lewis rat model was used to exclude immunological factors of graft deterioration. U-shaped ... [more] Objective: To describe a novel small animal model of tissue engineered aortic valved conduits aimed to investigate biological processes in an accelerated and inexpensive fashion. Methods: An isogenic Lewis to Lewis rat model was used to exclude immunological factors of graft deterioration. U-shaped aortic valvular grafts were decellularized and characterised morphologically. Acellular conduits were repopulated with labelled isogenic cells in a bioreactor under flow conditions. Grafts were anastomosed to the recipient's abdominal aorta in an end-to-side manner (n=7). Native rat aortas were implanted as a control group (n=7). Grafts were explanted after 28 days and characterized. Results: After treatment with Trypsin-EDTA, no residual cells were visualized in the scaffold. Mean DNA content decreased from 0.347 to 0 microg/mg DNA/tissue, the content of collageneous connective tissue and proteoglycans appeared slightly reduced. Isolated aortic rat endothelial cells and myofibroblasts were repopulated on the acellularized scaffold, florescent labelled myofibroblasts were identified in the meshwork. Endothelial cells formed a monolayer on the luminal surface. Reseeded cells were viable as ascertained by MTS assay. After implantation, Doppler and M-mode echography proofed pulsatile cusp movement. All conduits were patent after 28 days. Examination of tissue engineered explants revealed thickened aortic wall and incompetent valve function. Microscopically, aortic intima and media appeared normal, while the adventitia showed hyperproliferation of fibroblasts. Conclusions: Our new model leads to accelerated and reproducible results, suited for investigation of biological patterns of tissue engineering. The observed adventitial fibrosis emphasize the importance of careful selection of the optimal cell types for repopulation in tissue engineered constructs.

• Response to Letter Regarding Article, "Oxidant Stress Impairs In Vivo Reendothelialization Capacity of Endothelial Progenitor Cells From Patients With Type 2 Diabetes Mellitus: Restoration by the Peroxisome Proliferator- Activated Receptor-{gamma} Agonist

  S. A. Sorrentino, C. Besler, M. Muller, S. Schulz, N. Kirchhoff, C. Doerries, T. Horvath, A. Limbourg, F. Limbourg, H. Drexler, et al.

  Circulation. 01/2008; 117:e186.

• Extended-Release Niacin Improves Endothelial Function, Re-Endothelialization Capacity of Endothelial Progenitor Cells and Vasoprotective Properties of HDL in Patients with Metabolic Syndrome.

  S.A. Sorrentino, C. Besler, F. H. Bahlmann, M. Meyer, M. Mueller, T. Horváth, M. Heinemann, S. Flemmer, M.J. Bahr, H. Haller, H. Drexler, Landmesser U.

  AHA Scientific Sessions, Orlando, FL, USA; 11/2007

• High Density Lipoprotein (HDL) restores impairment of endothelial progenitor cells from patients with metabolic syndrome via NAD(P)H oxidase inhibition.

  S.A. Sorrentino, C. Besler, F. H. Bahlmann, M. Meyer, M. Mueller, S. Flemmer, H. Haller, H. Drexler, Landmesser U.

  European Society of Cardiology Congress, Wien, Austria; 09/2007

• Nebivolol Compared to Metoprolol-Succinate Improves Endothelial Function, Endothelial Progenitor Cell Mobilization, Left Ventricular Remodeling and Dysfunction Early After Myocardial Infarction

  S.A. Sorrentino, C. Doerries, W. Mohmand, R. Akbar, C. Besler, A. Schaefer, H. Drexler, U. Landmesser

  European Society of Cardiology Congress, Wien, Austria; 09/2007
• 14.82

  Impact points

  Oxidant stress impairs in vivo reendothelialization capacity of endothelial progenitor cells from patients with type 2 diabetes mellitus: restoration by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone.

  Sajoscha A Sorrentino, Ferdinand H Bahlmann, Christian Besler, Maja Müller, Svenja Schulz, Nina Kirchhoff, Carola Doerries, Tibor Horváth, Anne Limbourg, Florian Limbourg, Danilo Fliser, Hermann Haller, Helmut Drexler, Ulf Landmesser

  Circulation. 07/2007; 116(2):163-73.

  BACKGROUND: Endothelial progenitor cells (EPCs) are thought to contribute to endothelial recovery after arterial injury. We therefore compared in vivo reendothelialization capacity of EPCs derived from patients with diabetes mellitus and healthy subjects. Moreover, we examined the effect of treatmen... [more] BACKGROUND: Endothelial progenitor cells (EPCs) are thought to contribute to endothelial recovery after arterial injury. We therefore compared in vivo reendothelialization capacity of EPCs derived from patients with diabetes mellitus and healthy subjects. Moreover, we examined the effect of treatment with the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone on oxidant stress, nitric oxide (NO) bioavailability, and the in vivo reendothelialization capacity of EPCs from diabetic individuals. METHODS AND RESULTS: In vivo reendothelialization capacity of EPCs from diabetic patients (n=30) and healthy subjects (n=10) was examined in a nude mouse carotid injury model. Superoxide and NO production of EPCs was determined by electron spin resonance spectroscopy. Thirty patients with diabetes mellitus were randomized to 2 weeks of rosiglitazone (4 mg BID p.o.) or placebo treatment. In vivo reendothelialization capacity of EPCs derived from diabetic subjects was severely reduced compared with EPCs from healthy subjects (reendothelialized area: 8+/-3% versus 37+/-10%; P<0.001). EPCs from diabetic individuals had a substantially increased superoxide production and impaired NO bioavailability. Small-interfering RNA silencing of NAD(P)H oxidase subunit p47(phox) reduced superoxide production and restored NO bioavailability and in vivo reendothelialization capacity of EPCs from diabetic patients. Importantly, rosiglitazone therapy normalized NAD(P)H oxidase activity, restored NO bioavailability, and improved in vivo reendothelialization capacity of EPCs from diabetic patients (reendothelialized area: placebo versus rosiglitazone, 8+/-1% versus 38+/-5%; P<0.001). CONCLUSIONS: In vivo reendothelialization capacity of EPCs derived from individuals with diabetes mellitus is severely impaired at least partially as a result of increased NAD(P)H oxidase-dependent superoxide production and subsequently reduced NO bioavailability. Rosiglitazone therapy reduces NAD(P)H oxidase activity and improves reendothelialization capacity of EPCs from diabetic individuals, representing a potential novel mechanism whereby peroxisome proliferator-activated receptor-gamma agonism promotes vascular repair.
• 7.24

  Impact points

  Angiotensin II induces endothelial xanthine oxidase activation: role for endothelial dysfunction in patients with coronary disease.

  Ulf Landmesser, Stephan Spiekermann, Christoph Preuss, Sajoscha Sorrentino, Dieter Fischer, Costantina Manes, Maja Mueller, Helmut Drexler

  Arteriosclerosis, thrombosis, and vascular biology. 05/2007; 27(4):943-8.

  OBJECTIVE: Xanthine oxidase (XO), a major source of superoxide, has been implicated in endothelial dysfunction in atherosclerosis. Mechanisms, however, leading to endothelial XO activation remain poorly defined. We tested the effect of angiotensin II (Ang II) on endothelial XO and its relevance for ... [more] OBJECTIVE: Xanthine oxidase (XO), a major source of superoxide, has been implicated in endothelial dysfunction in atherosclerosis. Mechanisms, however, leading to endothelial XO activation remain poorly defined. We tested the effect of angiotensin II (Ang II) on endothelial XO and its relevance for endothelial dysfunction in patients with coronary disease. METHODS AND RESULTS: XO protein levels and XO-dependent superoxide production were determined in cultured endothelial cells in response to Ang II. In patients with coronary disease, endothelium-bound XO activity as determined by ESR spectroscopy and endothelium-dependent vasodilation were analyzed before and after 4 weeks of treatment with the AT1-receptor blocker losartan, the XO inhibitor allopurinol, or placebo. Ang II substantially increased endothelial XO protein levels and XO-dependent superoxide production in cultured endothelial cells, which was prevented by NAD(P)H-oxidase inhibition. In vivo, endothelium-bound XO activity was reduced by losartan and allopurinol, but not placebo therapy in patients with coronary disease. XO inhibition with oxypurinol improved endothelium-dependent vasodilation before, but not after losartan or allopurinol therapy. CONCLUSIONS: These findings suggest a novel mechanism whereby Ang II promotes endothelial oxidant stress, ie, by redox-sensitive XO activation. In patients with coronary disease, losartan therapy reduces endothelium-bound XO activity likely contributing to improved endothelial function.

• Effekt von Nebivolol vs. Metoprolol-Succinat auf endothel-abhängige Vasodilatation, endotheliale Progenitorzellen, linksventrikuläres (LV) Remodeling und LV-Dysfunktion nach experimentellem Myokardinfarkt

  S. Sorrentino, C. Doerries, W. Mohmand, R. Akbar, A. Schaefer, H. Drexler, U. Landmeser

  73. Jahrestagung der Deutschen Gesellschaft für Kardiologie, Herz- und Kreislaufforschung, Mannheim, Germany; 04/2007

• Essentielle Rolle der Notch Signaltransduktion für Differenzierung und Funktion von endothelialen Progenitorzellen in vaskulärer Regeneration.

  M. Ploom, A. Limbourg, D. Elligsen, S. Sorrentino, F. Bahlmann, H. Drexler, F. Limbourg

  73. Jahrestagung der Deutschen Gesellschaft für Kardiologie, Herz- und Kreislaufforschung, Mannheim, Germany; 04/2007

• Lysophospholipid-Rezeptor S1P3-vermittelte Inhibition der NAD(P)H Oxidase durch HDL verbessert die Re-Endothelialisierungs-Kapazität endothelialer Progenitorzellen bei metabolischem Syndrom.

  S. Sorrentino, C. Besler, F. Bahlmann, M. Meyer, M. Mueller, M. Heinemann, M.J. Bahr, H. Drexler, U Landmeser

  73. Jahrestagung der Deutschen Gesellschaft für Kardiologie, Herz- und Kreislaufforschung, Mannheim, Germany; 04/2007
• 9.21

  Impact points

  Critical role of the NAD(P)H oxidase subunit p47phox for left ventricular remodeling/dysfunction and survival after myocardial infarction.

  Carola Doerries, Karsten Grote, Denise Hilfiker-Kleiner, Maren Luchtefeld, Arnd Schaefer, Steven M Holland, Sajoscha Sorrentino, Costantina Manes, Bernhard Schieffer, Helmut Drexler, Ulf Landmesser

  Circulation research. 03/2007; 100(6):894-903.

  Accumulating evidence suggests a critical role of increased reactive oxygen species production for left ventricular (LV) remodeling and dysfunction after myocardial infarction (MI). An increased myocardial activity of the NAD(P)H oxidase, a major oxidant enzyme system, has been observed in human hea... [more] Accumulating evidence suggests a critical role of increased reactive oxygen species production for left ventricular (LV) remodeling and dysfunction after myocardial infarction (MI). An increased myocardial activity of the NAD(P)H oxidase, a major oxidant enzyme system, has been observed in human heart failure; however, the role of the NAD(P)H oxidase for LV remodeling and dysfunction after MI remains to be determined. MI was induced in wild-type (WT) mice (n=46) and mice lacking the cytosolic NAD(P)H oxidase component p47(phox) (p47(phox)-/- mice) (n=32). Infarct size was similar among the groups. NAD(P)H oxidase activity was markedly increased in remote LV myocardium of WT mice after MI as compared with sham-operated mice (83+/-8 versus 16.7+/-3.5 nmol of O(2)(-) x microg(-1) x min(-1); P<0.01) but not in p47(phox)-/- mice after MI (13.5+/-3.6 versus 15.5+/-3.5 nmol of O(2)(-) x microg(-1) x min(-1)), as assessed by electron-spin resonance spectroscopy using the spin probe CP-H. Furthermore, increased myocardial xanthine oxidase activity was observed in WT, but not in p47(phox)-/- mice after MI, suggesting NAD(P)H oxidase-dependent xanthine oxidase activation. Myocardial reactive oxygen species production was increased in WT mice, but not in p47(phox)-/- mice, after MI. LV cavity dilatation and dysfunction 4 weeks after MI were markedly attenuated in p47(phox)-/- mice as compared with WT mice, as assessed by echocardiography (LV end-diastolic diameter: 4.5+/-0.2 versus 6.3+/-0.3 mm, P<0.01; LV ejection fraction, 35.8+/-2.5 versus 22.6+/-4.4%, P<0.05). Furthermore, cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis were substantially reduced in p47(phox)-/- mice as compared with WT mice. Importantly, the survival rate was markedly higher in p47(phox)-/- mice as compared with WT mice after MI (72% versus 48%; P<0.05). These results suggest a pivotal role of NAD(P)H oxidase activation and its subunit p47(phox) for LV remodeling/dysfunction and survival after MI. The NAD(P)H oxidase system represents therefore a potential novel therapeutic target to prevent cardiac failure after MI.

• High Density Lipoprotein Restores Impaired Re-Endothelialization Capacity of Endothelial Progenitor Cells from Patients with Metabolic Syndrome via Lysophospholipid Receptor S1P3-mediated NAD(P)H Oxidase Inhibition.

  S.A. Sorrentino, C. Besler, F. Bahlmann, M. Meyer, M. Mueller, M. Heinemann, M. Sieniawski, S. Flemmer, M.J. Bahr, H. Haller, H. Drexler, U Landmeser

  AHA Scientific Sessions, Chicago, IL, USA; 11/2006

• Critical Role of the NAD(P)H Oxidase Subunit p47phox for LV-Remodeling, -Dysfunction and Survival post-Myocardial Infarction

  U. Landmesser, C. Doerries, K. Grote, S.A. Sorrentino, D. Hilfiker-Kleiner, M. Luchtefeld, A. Schaefer, S.M. Holland, B. Schieffer, H Drexler

  AHA Scientific Sessions, Chicago, IL, USA; 11/2006

• Effect of Nebivolol vs. Metoprolol on Endothelial Function, Endothelial Progenitor Cell Mobilization and Left Ventricular Remodeling and Dysfunction Early After Myocardial Infarction

  S.A. Sorrentino, C. Doerries, W. Mohmand, R. Akbar, C. Besler, A. Schaefer, H. Drexler, U Landmeser

  AHA Scientific Sessions, Chicago, IL, USA; 11/2006

• Eine Therapie mit dem PPAR-gamma Agonisten Rosiglitazon steigert die beeinträchtigte in vivo Re-Endothelialisierungs-Kapazität und NO Produktion endothelialer Progenitorzellen (EPC) von Patienten mit Typ 2 Diabetes mellitus

  S.A. Sorrentino, F.H. Bahlmann, C. Besler, M. Mueller, S. Schulz, N. Kirchhoff, D. Fliser, H. Drexler, U Landmesser

  22. Kardiologen-Physiologen Workshop "Zell-Zell-Wechselwirkungen im kardiovaskulären System", Würzburg, Germany; 10/2006