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Publications



Prof. Dr. Daniela Wenzel

2024

[1]
A. Brückner u. a., „Site-specific genetic and functional signatures of aortic endothelial cells at aneurysm predilection sites in healthy and AngII ApoE−/− mice“, Angiogenesis, Bd. 2024, Juli 2024, doi: 10.1007/s10456-024-09933-9.
[2]
A. Seidinger u. a., „Pharmacological Gq inhibition induces strong pulmonary vasorelaxation and reverses pulmonary hypertension“, EMBO molecular medicine / European Molecular Biology Organization, Bd. 16, Nr. 6, S. 1930–1956, Juli 2024, doi: 10.1038/s44321-024-00096-0.

2023

[1]
C. Biederbick u. a., „Combined use of magnetic microbeads for endothelial cell isolation and enhanced cell engraftment in myocardial repair“, Theranostics, Bd. 13, Nr. 3, S. 1150–1164, Feb. 2023, doi: 10.7150/thno.75871.

2022

[1]
A. Ghigo u. a., „A PI3Kγ mimetic peptide triggers CFTR gating, bronchodilation, and reduced inflammation in obstructive airway diseases“, Science translational medicine, Bd. 14, Nr. 638, Art. Nr. abl6328, März 2022, doi: 10.1126/scitranslmed.abl6328.
[2]
A. Simon, T. von Einem, A. Seidinger, M. Matthey, L. Bindila, und D. Wenzel, „The endocannabinoid anandamide is an airway relaxant in health and disease“, Nature communications, Bd. 13, Nr. 1, Art. Nr. 6941, Nov. 2022, doi: 10.1038/s41467-022-34327-0.
[3]
J. H. Voss u. a., „Imaging of Gαq proteins in mouse and human organs and tissues“, Pharmaceutics [ISSN: 1999-4923], Bd. 15, Nr. 1, S. 57, Dez. 2022, doi: 10.3390/pharmaceutics15010057.

2021

[1]
J. G. Schlegel u. a., „Macrocyclic Gq protein inhibitors FR900359 and/or YM-254890 – fit for translation?“,   ACS pharmacology & translational science , Bd. 4, Nr. 2, S. 888–897, Feb. 2021, doi: 10.1021/acsptsci.1c00021.
[2]
S. Rieck u. a., „Inhibition of vascular growth by modulation of the anandamide/fatty acid amide hydrolase axis“, Arteriosclerosis, thrombosis, and vascular biology, Bd. 41, Nr. 12, S. 2974–2989, Okt. 2021, doi: 10.1161/atvbaha.121.316973.

2020

[1]
M. Kuschak u. a., „Sensitive LC-MS/MS method for the quantification of Macrocyclic Gαq protein inhibitors in biological samples“, Frontiers in chemistry, Bd. 8, Art. Nr. 833, Sep. 2020, doi: 10.3389/fchem.2020.00833.
[2]
L. K. Pallos u. a., „Characterization of a pulmonary hypertension model caused by left heart disease in mouse“, The thoracic and cardiovascular surgeon, Bd. 68, Nr. Suppl. 1, S. S1–S72, März 2020, doi: 10.1055/s-0040-1705471.
[3]
B. Tosetti u. a., „A tissue‐specific screen of ceramide expression in aged mice identifies ceramide synthase‐1 and ceramide synthase‐5 as potential regulators of fiber size and strength in skeletal muscle“, Aging cell, Bd. 19, Nr. 1, Art. Nr. e13049, 2020, doi: 10.1111/acel.13049.
[4]
E. M. Pfeil u. a., „Heterotrimeric G protein subunit Gαq is a master switch for Gβγ-mediated calcium mobilization by Gi-coupled GPCRs“, 5. Mai 2020.
[5]
E. M. Pfeil u. a., „Heterotrimeric G protein subunit Gαq is a master switch for Gβγ-mediated calcium mobilization by Gi-Coupled GPCRs“, Molecular cell, Bd. 80, Nr. 6, S. 940-954.e6, Nov. 2020, doi: 10.1016/j.molcel.2020.10.027.

2019

[1]
M. Kuschak u. a., „Cell-permeable high-affinity tracers for Gq proteins provide structural insights, reveal distinct binding kinetics and identify small molecule inhibitors“, British journal of pharmacology, Bd. 177, Nr. 8, S. 1898–1916, Dez. 2019, doi: 10.1111/bph.14960.
[2]
S. Rieck u. a., „Local anti-angiogenic therapy by magnet-assisted downregulation of SHP2 phosphatase“, Journal of controlled release, Bd. 305, S. 155–164, 2019, doi: 10.1016/j.jconrel.2019.05.031.

2018

[1]
A. Ottersbach u. a., „Improved heart repair upon myocardial infarction: combination of magnetic nanoparticles and tailored magnets strongly increases engraftment of myocytes“, Biomaterials, Bd. 155, S. 176–190, 2018, doi: 10.1016/j.biomaterials.2017.11.012.
[2]
G. D. Duerr u. a., „CB2-deficiency is associated with a stronger hypertrophy and remodeling of the right ventricle in a murine model of left pulmonary artery occlusion“, Life sciences, Bd. 215, S. 96–105, 2018, doi: 10.1016/j.lfs.2018.11.003.
[3]
K. Herz u. a., „Visualization of endothelial cell cycle dynamics in mouse using the Flt-1/eGFP-anillin system“, Angiogenesis, Bd. 21, Nr. 2, S. 349–361, 2018, doi: 10.1007/s10456-018-9601-1.
[4]
A. Olschewski u. a., „Pathobiology, pathology and genetics of pulmonary hypertension: update from the Cologne Consensus Conference 2018“, International journal of cardiology, Bd. 272, Nr. Suppl., S. 4–10, 2018, doi: 10.1016/j.ijcard.2018.09.070.
[5]
M. Breitbach u. a., „In vivo labeling by CD73 marks multipotent stromal cells and highlights endothelial heterogeneity in the bone marrow niche“, Cell stem cell, Bd. 22, Nr. 2, S. 262–276, 2018, doi: 10.1016/j.stem.2018.01.008.
[6]
V. Neumann u. a., „The β2 agonist terbutaline specifically decreases pulmonary arterial pressure under normoxia and hypoxia via α adrenoceptor antagonism“, The FASEB journal / Federation of American Societies for Experimental Biology, Bd. 32, Nr. 5, S. 2519–2530, 2018, doi: 10.1096/fj.201700684rr.
[7]
M. Crüsemann u. a., „Heterologous expression, biosynthetic studies, and ecological function of the selective Gq-signaling inhibitor FR900359“, Angewandte Chemie International edition, Bd. 57, Nr. 3, S. 836–840, 2018, doi: 10.1002/anie.201707996.
[8]
F. Winkler u. a., „PECAM/eGFP transgenic mice for monitoring of angiogenesis in health and disease“, Scientific reports, Bd. 8, Nr. 1, Art. Nr. 17582, 2018, doi: 10.1038/s41598-018-36039-2.
[9]
D. Wenzel u. a., „Inhibition of Gq signaling induces airway relaxation in mouse models of asthma“, American journal of respiratory and critical care medicine, Bd. 197. American Thoracic Society, New York, NY, S. A1231, 2018.

2017

[1]
W. K. Seemann u. a., „Engineered context-sensitive agonism: tissue-selective drug signaling through a G protein-coupled receptor“, The journal of pharmacology and experimental therapeutics, Bd. 360, Nr. 2, S. 289–299, 2017, doi: 10.1124/jpet.116.237149.
[2]
C. Engel u. a., „RIG-I resists hypoxia-induced immunosuppression and dedifferentiation“, Cancer immunology research, Bd. 5, Nr. 6, S. 455–467, 2017, doi: 10.1158/2326-6066.cir-16-0129-t.
[3]
F. Jansen u. a., „Intercellular transfer of miR-126-3p by endothelial microparticles reduces vascular smooth muscle cell proliferation and limits neointima formation by inhibiting LRP6“, Journal of molecular and cellular cardiology, Bd. 104, S. 43–52, 2017, doi: 10.1016/j.yjmcc.2016.12.005.
[4]
Y. Heun u. a., „Targeting of magnetic nanoparticle-coated microbubbles to the vascular wall empowers site-specific lentiviral gene delivery in vivo“, Theranostics, Bd. 7, Nr. 2, S. 295–307, 2017, doi: 10.7150/thno.16192.
[5]
B. Kathage u. a., „The cochaperone BAG3 coordinates protein synthesis and autophagy under mechanical strain through spatial regulation of mTORC1“, Biochimica et biophysica acta Molecular cell research, Bd. 1864, Nr. 1, S. 62–75, 2017, doi: 10.1016/j.bbamcr.2016.10.007.
[6]
M. Matthey u. a., „The pharmacological Gq inhibitor FR900359 abrogates airway hyperresponsiveness in different asthma models“, Acta physiologica Supplement, Bd. 219, Nr. 711. John Wiley and Sons, Oxford, S. 64, 2017.
[7]
A. Seidinger, M. Matthey, G. König, E. Kostenis, B. K. Fleischmann, und D. Wenzel, „Inhibitory effects of uromodulin on phosphate-induced osteo-/chondrogenic transformation and calcification of vascular smooth muscle cells“, Acta physiologica Supplement, Bd. 219, Nr. 711. John Wiley and Sons, Oxford, S. B04-2, 2017.
[8]
A. Seidinger, M. Matthey, G. König, E. Kostenis, B. K. Fleischmann, und D. Wenzel, „The Gq protein inhibitor FR900359 induces strong vasodilation in pulmonary arteries“, Acta physiologica Supplement, Bd. 219, Nr. 711. John Wiley and Sons, Oxford, S. 137, 2017.
[9]
M. Matthey u. a., „Targeted inhibition of Gq signaling induces airway relaxation in mouse models of asthma“, Science translational medicine, Bd. 9, Nr. 407, Art. Nr. eaag2288, 2017, doi: 10.1126/scitranslmed.aag2288.
[10]
D. Wenzel, M. Matthey, E. Silantyeva, L. Wohn, und B. K. Fleischmann, „Inhibition of fatty acid amide hydrolase (faah) prevents pulmonary hypertension via activation of Cb2 receptors“, American journal of respiratory and critical care medicine, Bd. 195. American Thoracic Society, New York, NY, S. A4192, 2017.

2016

[1]
M. Matthey u. a., „The pharmacological Gq inhibitor FR900359 induces airway relaxation without systemic side effects“, Acta physiologica Supplement, Bd. 216, Nr. 707. John Wiley and Sons, Oxford, S. OS08-7, 2016.
[2]
F. Winkler u. a., „Endothelial cell labeling and magnet-assisted purification using a transgenic PECAM/eGFP mouse model“, Acta physiologica Supplement, Bd. 216, Nr. 707. John Wiley and Sons, Oxford, S. OS12-7, 2016.
[3]
D. Wenzel, „Magnetic nanoparticles: novel options for vascular repair?“, Nanomedicine, Bd. 11, Nr. 8, S. 869–872, 2016, doi: 10.2217/nnm-2016-0031.
[4]
D. Wenzel, „Nanomedicine: vascular repair by circumferential gene and endothelial cell therapy“, Acta physiologica Supplement, Bd. 216, Nr. 707. John Wiley and Sons, Oxford, S. PS02-7, 2016.
[5]
S. Vosen u. a., „Improvement of vascular function by magnetic nanoparticle-assisted circumferential gene transfer into the native endothelium“, Journal of controlled release, Bd. 241, S. 164–173, 2016, doi: 10.1016/j.jconrel.2016.09.024.
[6]
S. Vosen u. a., „Vascular repair by circumferential cell therapy using magnetic nanoparticles and tailored magnets“, ACS nano / American Chemical Society, Bd. 10, Nr. 1, S. 369–376, 2016, doi: 10.1021/acsnano.5b04996.
[7]
S. Annala u. a., „FR900359: a cyclic depsipeptide to explore the role of Gq proteins in biological systems“, Naunyn-Schmiedeberg’s archives of pharmacology, Bd. 389, Nr. Suppl. 1. Springer, Berlin, S. S31, 2016.
[8]
K. M. Kniewallner, D. Wenzel, und C. Humpel, „Thiazine Red+ platelet inclusions in cerebral blood vessels are first signs in an Alzheimer’s disease mouse model“, Scientific reports, Bd. 6, Nr. 1, Art. Nr. 28447, 2016, doi: 10.1038/srep28447.
[9]
A. Olschewski u. a., „Pathobiologie, Pathologie und Genetik der pulmonalen Hypertonie: Empfehlungen der Kölner Konsensus-Konferenz 2016“, Deutsche medizinische Wochenschrift, Bd. 141, Nr. Suppl. 1, S. S4–S9, 2016, doi: 10.1055/s-0042-114520.

2015

[1]
M. Matthey u. a., „Inhibition of fatty acid amide hydrolase (FAAH) prevents pulmonary hypertension“, Acta physiologica Supplement, Bd. 213, Nr. 699. John Wiley and Sons, Oxford, S. 49, 2015.
[2]
I. Tuleta u. a., „Intermittent hypoxia impairs endothelial function in early preatherosclerosis“, in Pulmonary function, Bd. 858, M. Pokorski, Hrsg. Cham: Springer, 2015, S. 1–7. doi: 10.1007/5584_2015_114.
[3]
F. Winkler u. a., „Characterization of endothelial cell-specific PECAM/eGFP expression in a transgenic mouse model“, Acta physiologica Supplement, Bd. 213, Nr. 699. John Wiley and Sons, Oxford, S. 92, 2015.
[4]
R. Schrage u. a., „The experimental power of FR900359 to study Gq-regulated biological processes“, Nature communications, Bd. 6, Nr. 1, Art. Nr. 10156, 2015, doi: 10.1038/ncomms10156.

2014

[1]
A.-L. Schmitz u. a., „A cell-permeable inhibitor to trap Gαq proteins in the empty pocket conformation“, Chemistry & biology, Bd. 21, Nr. 7, S. 890–902, 2014, doi: 10.1016/j.chembiol.2014.06.003.
[2]
G. D. Duerr u. a., „The endocannabinoid-CB2 receptor axis protects the ischemic heart at the early stage of cardiomyopathy“, Basic research in cardiology, Bd. 109, Nr. 4, S. 425, 2014, doi: 10.1007/s00395-014-0425-x.
[3]
I. Tuleta u. a., „Hypoxia-induced endothelial dysfunction in apolipoprotein E-deficient mice; effects of infliximab and l-glutathione“, Atherosclerosis, Bd. 236, Nr. 2, S. 400–410, 2014, doi: 10.1016/j.atherosclerosis.2014.08.021.
[4]
M. Matthey u. a., „The endocannabinoid anandamide regulates pulmonary arterial pressure under physiological and pathophysiologocal conditions“, Acta physiologica Supplement, Bd. 210, Nr. 695. John Wiley and Sons, Oxford, S. 40, 2014.
[5]
J. Welschoff, M. Matthey, und D. Wenzel, „RGD peptides induce relaxation of pulmonary arteries and airways via β3-integrins“, The FASEB journal / Federation of American Societies for Experimental Biology, Bd. 28, Nr. 5, S. 2281–2292, 2014, doi: 10.1096/fj.13-246348.
[6]
S. Koster u. a., „Modulation of angiogenesis by the fatty acid amide hydrolase (FAAH)“, Acta physiologica Supplement, Bd. 210, Nr. 695. John Wiley and Sons, Oxford, S. 120, 2014.
[7]
C. S. Clemen u. a., „The toxic effect of R350P mutant desmin in striated muscle of man and mouse“, Acta neuropathologica, Bd. 129, Nr. 2, S. 297–315, 2014, doi: 10.1007/s00401-014-1363-2.
[8]
T. Bald u. a., „Ultraviolet-radiation-induced inflammation promotes angiotropism and metastasis in melanoma“, Nature, Bd. 507, Nr. 7490, S. 109–113, 2014, doi: 10.1038/nature13111.
[9]
D. Wenzel u. a., „The endocannabinoid anandamide mediates hypoxic pulmonary vasoconstriction and pulmonary hypertension“, American journal of respiratory and critical care medicine, Bd. 189. American Thoracic Society, New York, NY, S. A5558, 2014.

2013

[1]
F. Jansen u. a., „Endothelial microparticle–mediated transfer of microRNA-126 promotes vascular endothelial cell repair via SPRED1 and is abrogated in glucose-damaged endothelial microparticles“, Circulation, Bd. 128, Nr. 18, S. 2026–2038, 2013, doi: 10.1161/circulationaha.113.001720.
[2]
S. Rieck, K. Zimmermann, und D. Wenzel, „Transduction of murine embryonic stem cells by magnetic nanoparticle-assisted lentiviral gene transfer“, in Stem cell nanotechnology, Bd. 1058, K. Turksen, Hrsg. New York: Humana Press Inc., 2013, S. 89–96. doi: 10.1007/7651_2013_6.
[3]
T. Bruegmann, S. Vosen, D. Wenzel, B. K. Fleischmann, und P. Sasse, „Optogenetic control of vascular tone with high temporal resolution“, Biophysical journal, Bd. 104, Nr. 2, Suppl. 1. Biophysical Society, Bethesda, Md., S. 678A, 2013. doi: 10.1016/j.bpj.2012.11.3742.
[4]
D. Wenzel u. a., „Endocannabinoid anandamide mediates hypoxic pulmonary vasoconstriction“, Proceedings of the National Academy of Sciences of the United States of America, Bd. 110, Nr. 46, S. 18710–18715, 2013, doi: 10.1073/pnas.1308130110.
[5]
D. Wenzel u. a., „The beta 2-adrenoceptor agonist terbutaline specifically decreases pulmonary arterial pressure by alpha-adrenoceptor antagonism“, American journal of respiratory and critical care medicine, Bd. 187. American Thoracic Society, New York, NY, S. A 2270, 2013.

2012

[1]
D. Wenzel, M. Koch, M. Matthey, J. C. Heinemann, und B. K. Fleischmann, „Identification of a novel vasoconstrictor peptide specific for the systemic circulation“, Hypertension, Bd. 59, Nr. 6, S. 1256–1262, 2012, doi: 10.1161/hypertensionaha.111.188367.
[2]
D. Wenzel u. a., „Identification of magnetic nanoparticles for combined positioning and lentiviral transduction of endothelial cells“, Pharmaceutical research, Bd. 29, Nr. 5, S. 1242–1254, 2012, doi: 10.1007/s11095-011-0657-5.
[3]
K. Herz u. a., „Live monitoring of small vessels during development and disease using the flt-1 promoter element“, Basic research in cardiology, Bd. 107, Nr. 2, Art. Nr. 0257, 2012, doi: 10.1007/s00395-012-0257-5.
[4]
C. Trueck u. a., „Optimization of magnetic nanoparticle-assisted lentiviral gene transfer“, Pharmaceutical research, Bd. 29, Nr. 5, S. 1255–1269, 2012, doi: 10.1007/s11095-011-0660-x.
[5]
G. D. Duerr u. a., „Endocannabinoids and cannabinoid receptor CB2 act cardioprotective in a murine model of ischemic cardiomyopathy“, Cardiovascular research, Bd. 93, Nr. Suppl. 1. Oxford Univ. Pr., Oxford, S. S49, 2012.
[6]
A. Heidsieck, S. Vosen, K. Zimmermann, D. Wenzel, und B. Gleich, „Analysis of trajectories for targeting of magnetic nanoparticles in blood vessels“, Molecular pharmaceutics, Bd. 9, Nr. 7, S. 2029–2038, 2012, doi: 10.1021/mp3001155.

2011

[1]
R. Knies u. a., „Verminderung des Gefäßtonus im pulmonal-arteriellen Gefäßsystem durch den spezifischen β2-Adrenozeptor-Blocker ICI 118,551 im Mausmodell“, Pneumologie, Bd. 65, S. S135, Nov. 2011, doi: 10.1055/s-0030-1256825.
[2]
V. Stolle u. a., „The beta 2-adrenoceptor agonist terbutaline specifically decreases pulmonary arterial pressure by alpha-adrenoceptor antagonism“, The thoracic and cardiovascular surgeon, Bd. 59, Nr. Suppl. 1. Thieme Verlag, Stuttgart, 1. Februar 2011. doi: 10.1055/s-0030-1269297.
[3]
T. Bruegmann u. a., „Optogenetics in cardiovascular research: a new tool for light-induced depolarization of cardiomyocytes and vascular smooth muscle cells in vitro and in vivo“, European heart journal Supplements, Bd. 32, Nr. Suppl. 1. Oxford University Press, Oxford, S. 997, 2011.
[4]
D. Wenzel u. a., „Radially symmetric endothelial cell replacement and lentiviral targeting in vessels by the use of magnetic nanoparticles (MNPs)“, The FASEB journal / Federation of American Societies for Experimental Biology, Bd. 25. FASEB, Bethesda, Md, 2011.
[5]
I. Tuleta u. a., „Impairment of endothelial function by chronic intermittent hypoxia in ApoE-/- mice - implications for anti-inflammatory and anti-oxidative treatment“, The European respiratory journal Supplement, Bd. 40, Nr. Suppl. 56. Munksgaard, Copenhagen, S. 3647, 2011.
[6]
W. Seemann u. a., „Dualsteric GPCR-targeting: whole cell response to M-2 receptor activation is cell type-dependent“, Naunyn-Schmiedeberg’s archives of pharmacology, Bd. 383, Nr. Suppl. 1. Springer, Berlin, S. 58, 2011.
[7]
A. Pfeifer u. a., „Targeted delivery of viral vectors and cells by magnetic nanoparticles“, Journal of vascular research, Bd. 48, Nr. Suppl. 1. Karger, Basel, S. 65, 2011.

2010

[1]
J. Günther, K. Schulte, D. Wenzel, B. Malinowska, und E. Schlicker, „Prostaglandins of the E series inhibit monoamine release via EP3 receptors: proof with the competitive EP3 receptor antagonist L-826,266“, Naunyn-Schmiedeberg’s archives of pharmacology, Bd. 381, Nr. 1, S. 21–31, 2010, doi: 10.1007/s00210-009-0478-9.
[2]
D. Malan u. a., „Endothelial β1 integrins regulate sprouting and network formation during vascular development“, Development, Bd. 137, Nr. 6, S. 993–1002, 2010, doi: 10.1242/dev.045377.
[3]
D. Wenzel u. a., „Endothelial beta1 integrins regulate sprouting and network formation during vascular development“, The FASEB journal / Federation of American Societies for Experimental Biology, Bd. 24. FASEB, Bethesda, Md, 2010.
[4]
W. Seemann u. a., „Biased signaling of a dualsteric muscarinic agonist in spontaneously contracting atrial cardiomyocytes“, Naunyn-Schmiedeberg’s archives of pharmacology, Bd. 381, Nr. Suppl. 1. Springer, Berlin, S. 12, 2010.
[5]
V. Arndt u. a., „Chaperone-assisted selective autophagy is essential for muscle maintenance“, Current biology, Bd. 20, Nr. 2, S. 143–148, 2010, doi: 10.1016/j.cub.2009.11.022.

2009

[1]
G. Zolles u. a., „Association with the auxiliary subunit PEX5R/Trip8b controls responsiveness of HCN channels to cAMP and adrenergic stimulation“, Neuron, Bd. 62, Nr. 6, S. 814–825, 2009, doi: 10.1016/j.neuron.2009.05.008.
[2]
D. Wenzel u. a., „β 2 -adrenoceptor antagonist ICI 118,551 decreases pulmonary vascular tone in mice via a G ( i/o) protein/nitric oxide-coupled pathway“, Hypertension, Bd. 54, Nr. 1, S. 157–163, 2009, doi: 10.1161/hypertensionaha.109.130468.
[3]
C. Trueck u. a., „Targeting of lentiviral vectors and positioning of transduced cells by magnetic nanoparticles“, Human gene therapy, Bd. 20, Nr. 11. Liebert, New York, NY, S. 1386, 2009.
[4]
W. Röll u. a., „Zellersatztherapie am Herzen: Fiktion oder reale Möglichkeit. Eine tierexperimentelle Annäherung“, Zeitschrift für Herz-, Thorax- und Gefäßchirurgie, Bd. 23, Nr. 3, S. 170–176, 2009, doi: 10.1007/s00398-009-0719-8.
[5]
R. Knies u. a., „The beta 2-adrenoreceptor antagonist ICI 118,551 reduces the pulmonary artery vascular tone by a Gi/o-protein/NO-independent signal pathway in the mouse model“, Clinical research in cardiology, Bd. 98, Nr. 9. Springer-Medizin Verlag, Heidelberg, S. 589, 2009.
[6]
U. M. Becher, A. Hofmann, D. Wenzel, B. K. Fleischmann, G. Nickenig, und A. Pfeifer, „Positioning of transgenic endothelial cells to injured mouse carotid artery by magnetic nanoparticles“, European heart journal Supplements, Bd. 30, Nr. Suppl. 1. Oxford University Press, Oxford, S. 177–178, 2009.
[7]
A. Hofmann u. a., „Combined targeting of lentiviral vectors and positioning of transduced cells by magnetic nanoparticles“, Proceedings of the National Academy of Sciences of the United States of America, Bd. 106, Nr. 1, S. 44–49, 2009, doi: 10.1073/pnas.0803746106.

2008

[1]
D. Wenzel u. a., „The beta 2-adrenoceptor terbutaline is a strong vasorelaxant of pulmonary arteries“, The FASEB journal / Federation of American Societies for Experimental Biology, Bd. 22. FASEB, Bethesda, Md, 2008.
[2]
R. Knies u. a., „An abatement of the vessel tonus in pulmonary arterial system“, Clinical research in cardiology, Bd. 97, Nr. 9. Springer-Medizin Verlag, Heidelberg, S. 705, 2008.

2007

[1]
R. Knies, D. Wenzel, J. Welschoff, V. Stolle, B. K. Fleischmann, und J. Breuter, „Role of beta(2) receptor agonists in the regulation of vascular tonus in pulmonary and systemic circulation“, Clinical research in cardiology, Bd. 96, Nr. 9. Springer-Medizin Verlag, Heidelberg, S. 671, 2007.

2006

[1]
D. Wenzel u. a., „Endostatin, the proteolytic fragment of collagen XVIII, induces vasorelaxation“, Circulation research, Bd. 98, Nr. 9, S. 1203–1211, 2006, doi: 10.1161/01.res.0000219899.93384.ed.
[2]
E. Kolossov u. a., „Engraftment of engineered ES cell–derived cardiomyocytes but not BM cells restores contractile function to the infarcted myocardium“, The Journal of experimental medicine, Bd. 203, Nr. 10, S. 2315–2327, 2006, doi: 10.1084/jem.20061469.
[3]
G. Zolles u. a., „Pacemaking by HCN channels requires interaction with phosphoinositides“, Neuron, Bd. 52, Nr. 6, S. 1027–1036, 2006, doi: 10.1016/j.neuron.2006.12.005.
[4]
A. Schmidt u. a., „Endostatin influences endothelial morphology via the activated ERK1/2-kinase endothelial morphology and signal transduction“, Microvascular research, Bd. 71, Nr. 3, S. 152–162, 2006, doi: 10.1016/j.mvr.2006.01.001.
[5]
R. Knies, D. Wenzel, B. K. Fleischmann, und J. Breuer, „Differences in adrenoceptor vascular tone regulation between systemic and pulmonary circulation“, Journal of vascular research, Bd. 43, Nr. 6. Karger, Basel, S. 542–543, 2006.

2005

[1]
A. Schmidt, D. Wenzel, I. Thorey, S. Werner, B. K. Fleischmann, und W. Bloch, „Endostatin down-regulates soluble guanylate cyclase (sGC) in endothelial cells in vivo: influence of endostatin on vascular endothelial growth factor (VEGF) signaling“, Endothelium, Bd. 12, Nr. 5–6, S. 251–257, 2005, doi: 10.1080/10623320500476690.
[2]
A. Schmidt, D. Wenzel, K. Addicks, B. K. Fleischmann, und W. Bloch, „Endostatin-mediated influence on endothelial morphology and VEGF signal transduction is mediated via the protein phosphatase 2A“, in Cardio-Visionen, Düsseldorf, 2005, S. 46–47.
[3]
A. Schmidt, D. Wenzel, B. K. Fleischmann, und W. Bloch, „The effect of endostatin is mediated by PP2A“, Journal of vascular research, Bd. 42, Nr. Suppl. 2. Karger, Basel, S. 96, 2005.

2004

[1]
J. Hescheler u. a., „Implication of therapeutic cloning for organ transplantation“, European journal of cardio-thoracic surgery, Bd. 26, Nr. Suppl. 1, S. S54–S55, 2004, doi: 10.1016/j.ejctsup.2004.11.014.
[2]
A. Schmidt u. a., „Influence of endostatin on embryonic vasculo- and angiogenesis“, Developmental dynamics, Bd. 230, Nr. 3, S. 468–480, 2004, doi: 10.1002/dvdy.20072.

2002

[1]
S. Kazemi u. a., „Differential role of bFGF and VEGF for vasculogenesis“, Cellular physiology and biochemistry, Bd. 12, Nr. 2–3, S. 55–62, 2002, doi: 10.1159/000063781.

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