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This profile was last updated on 5/5/12  and contains information from public web pages.

Prof. Thomas Walther

Wrong Prof. Thomas Walther?


Phone: +44 **** ******  HQ Phone
Email: t***@***.uk
Hull York Medical School
Hull Royal Infirmary Anlaby Road
Hull , E Riding of Yorkshire HU3 2JZ
United Kingdom

Company Description: The Hull York Medical School is a three-way partnership between the University of Hull, the University of York and the National Health Service within our region....   more

Employment History

19 Total References
Web References
Staff - Hull York Medical School [cached]
Professor Thomas Walther Professor in Cardiovascular Physiology
Molecular and vascular biology - Research at Hull York Medical School [cached]
Professor Thomas Walther Chair in Biomedical Sciences
Thomas Walther
Haemostasis and thrombosis - Research at Hull York Medical School [cached]
Professor Thomas Walther Chair in Biomedical Science
Thomas Walther
HYMS: research profile: Thomas Walther [cached]
Professor Thomas Walther HYMS: research profile: Thomas Walther
Group Leader: Professor Thomas Walther
Professor Thomas Walther
The main aim of Professor Thomas Walther's research is to improve the treatment of patients who suffer from cardiovascular conditions, by:
Professor Walther's research is particularly significant in the area of combining basic and translational research to improve the prediction and treatment of cardiovascular diseases. He follows the strategy of molecular investigation, followed by evaluation in experimental models, and finally establishing proof-of-concept in humans, aiming to find new therapeutic strategies.
Examples of detailed research areas
Professor Walther is investigating the role of three different peptide systems (renin-angiotensin system, kallikrein-kinin system, and natriuretic peptide system) in the aetiology of different diseases, mainly focused on cardiovascular pathophysiology in end-organs such as the brain or heart (for instance, Walther et al., FASEB J., 2002a, 2003, 2008). Having identified the intense interactions of these systems, he is interested in finding out how an imbalance of cross-talk can influence the development of heart failure and vascular diseases (for instance, Walther et al., FASEB J., 2002b; Tschöpe et al. and Walther, Cardiovasc. Res., 2004). These investigations are especially focused on altered gene regulation, modified receptor/receptor interaction, and receptor mediated intracellular signalling.
Professor Walther has hypothesised that angiotensin II could be a mediator between homeostatic changes in the vascular perfusion bed and growth factor driven angiogenesis. This resulted in the first evidence that angiogenesis is stimulated in vivo through the AT2 receptor system. Angiotensin II acts as a humoral regulator of peripheral angiogenesis, involving two receptor subtypes with opposing actions (Walther et al., FASEB J., 2003). Current studies aim to identify the cellular progenitors (stem cells) for vascular growth and regeneration under the control of angiotensin II.
He found new receptors which interact with the renin-angiotensin system and/or kallikrein-kinin system (e.g. Santos et al. & Walther, Proc. Natl. Acad. Sci. USA, 2003 Gembardt et al & Walther, Mol. Cell. Biochem., 2008) and which have a significant impact on neuronal and hormonal control under ischemic conditions.
Professor Walther's work has advanced the understanding of the natriuretic peptide system by identifying that brain natriuretic peptide (BNP) was resistant to neutral endopeptidase digestion. This led to identification of the peptidase that is responsible for BNP degradation which in turn opens up a new possibility of using pharmacological interventions to enhance the cardioprotective actions of BNP (Pankow et al. & Walther, Circulation Research., 2007).
Another aspect of Professor Walther's research is identifying and investigating new interactions between gene products (often newly identified G protein-coupled receptors) and their importance for functional cardiovascular deregulation. By identifying an interaction between the receptors Mas and AT1, he was the first to demonstrate that a G protein-coupled receptor could act as a physiological antagonist of a previously characterised receptor. This AT1-Mas complex also has potential as a drug target for developing new therapies for cardiovascular disease (Kostenis et al. & Walther, Circulation., 2005).
Professor Walther's further research investigates the claim that receptors (which may be of different receptor families) may physically interact within the cell membrane and influence each others' signalling pathways. Most recently, his group has discovered interactions between a G protein-coupled receptor and a membrane bound guanylate cyclase and shown cross-talk between their signalling in the heart (unpublished data).
Members of Prof. Walther's research group
Publications of the last 10 years: Prof. Thomas Walther
Group Leader: Professor Walther
Professor Walther's research group
Publications of the last 10 years: Prof. Thomas Walther
Publications of the last 10 years: ... [cached]
Publications of the last 10 years: Prof. Thomas Walther HYMS Research: Centre for Biomedical Research
Publications of the last 10 years: Prof. Thomas Walther
131. van Esch, J.H.M., Gembardt, F., Sterner-Kock, A., Heringer-Walther, S., Le, T.H., Laßner, D., Stijnen, T., Coffman, T.M., Schultheiss, H-P., Danser, A.H.J., and Walther, T. (2010). Cardiac phenotype and angiotensin II levels in AT1a, AT1b and AT2 receptor single, double and triple knockout mice. Cardiovasc. Res., in press (PMID: 20071356)
130. Koitka, A., Cao, Z., Koh, P., Watson, A.M., Sourris, K.C., Loufrani, L., Soro-Paavonen, A., Walther, T., Woollard, K.J., Jandeleit-Dahm, K.A., Cooper, M.E., and Allen T.J. (2010).
R., Walther, T., Gembardt, F., Smolders, I., Vanderheyden, P., Albiston, A.L., Chai, S.Y., and Dupont, A.G. (2010).
127. Kamilic, J., Hamming, I., Kreutz, R., Bolbrinker, J., Siems, W.-E., Nassar, I., Sluimer, J.C., Walther, T., Navis, G.J., and van Goor H. (2010).
126. Pankow, K., Schwiebs, A., Becker, M., Siems, W., Krause, G., Walther, T. (2009) Structural Substrate Conditions Required for Neutral Endopeptidase-mediated Natriuretic Peptide Degradation.
125. Davern, P.J., Chen, D., Head, G.A., Chavez, C.A., Walther, T., and Mayorov, D.N. (2009). Role of Angiotensin II Type 1A Receptors in Cardiovascular Reactivity and Neuronal Activation After Aversive Stress in Mice. Hypertension, 54, 1262-8.
124. Esteban, V., Heringer-Walther, S., Sterner-Kock, A., de Bruin, R., van den Engel, S., Wang, Y., Mezzano, S., Egido, J., Schultheiss, H.-P., Ruiz- Ortega, M., and Walther, T. (2009).
123. Pawlowski, T.L., Heringer-Walther, S., Cheng, C.-H., Archie, J.G., Chen, C.-F., Walther, T., and Srivastava, A.K. (2009). Candidate Agtr2 influenced genes and pathways identified by expression profiling in the developing brain of Agtr2-/y mice. Genomics, in press.
122. Heringer-Walther, S., Eckert, K., Schumacher, S.-M., Uharek, L., Wulf-Goldenberg, A., Gembardt, F., Fichtner, I., Schultheiss, H.-P., Rodgers, K., and Walther, T. (2009).
121. Chen, D., La Greca, L., Head, G.A., Walther, T., and Mayorov, D.N. (2009). Blood pressure reactivity to emotional stress is reduced in AT1A receptor knockout mice on normal, but not high salt intake. Hypertens. Res., 32, 559-64.
120. Westermann, D., Walther, T., Savvatis, K., Sobirey, M., Riad, A., Bader, M., Schultheiss, H.-P., and Tschöpe, C. (2009).
119. Walther, T., Albrecht, D., Becker, M., Schubert, M., Kouznetsova, E., Wiesner, B., Maul, B., Schliebs, R., Grecksch, G., Furkert, J., Sterner-Kock, A., Schultheiss, H.-P., Becker, A., and Siems W.-E. (2009).
117. Kluskens, L.D., Nelemans, A., Rink, R., de Vries, L., Meter-Arkema, A., Wang, Y., Walther, T., Kuipers, A., Moll, G.N., and Haas, M. (2009).
116. Xu, P., Wang, J., Sterner-Kock, A., Bader, M., Schultheiss, H.-P., and Walther, T. (2009).
115. Hansen, J.L. Hansen, J.T., Speerschneider, T., Lyngsø, C., Erikstrup, N., Burstein, E.S., Weiner, D.M., Walther, T., Makita, N., Iiri, T., Merten, N., Kostenis, E., and Sheikh, S.P. (2009).
114. Wang, Y., Ebermann, L., Sterner-Kock, A., Wika, S., Schultheiss, H.-P., Dörner, A. and Walther, T. (2009). Myocardial overexpression of adenine nucleotide translocase 1 ameliorates diabetic cardiomyopathy in mice. Exp. Physiol., 94 220-227.
113. Gembardt, F., Grajewski, S., Vahl, M., Schultheiss, H.-P., and Walther, T. (2008).
112. Mercure, C., Yogi, A., Callera, G.E., Aranha, A.B., Bader, M., Ferreira, A.J., Santos, R.A.S., Walther, T., Touyz, R.M., and Reudelhuber, T.L. (2008).
111. Walther, T., Jank, A., Heringer-Walther, S., Horn, L.-C., and Stepan, H. (2008).
110. Yousif, H., Benter, I.F., Abul, A.H., Abraham, S., Walther, T., and Akhtar, S. (2008). Inhibition of Ras-GTPase signaling by FPTIII ameliorates development of cardiovascular dysfunction in diabetic hypertensive rats. Vasc. Pharmacol., 49, 151-7.
109. Ebermann, L., Spillmann, F., Sidiropoulos, M., Escher, F., Heringer-Walther, S., Schultheiss, H.-P., Tschöpe, C., and Walther, T. (2008).
108. Gembardt, F., Heringer-Walther, S., van Esch, J.H.M., Sterner-Kock, A., van Veghel, R., Le, T.H., Garrelds, I.M., Coffman, T.M., Danser, A.H.J., Schultheiss, H.-P., and Walther, T. (2008). Cardiovascular phenotype of mice lacking all three subtypes of angiotensin II receptors. FASEB J., 22, 3068-77.
107. Karamyan, V.T., Gembardt, F., Rabey, F.R., Walther, T., Speth, R.C. (2008). Characterization of the brain-specific non-AT1, non-AT2 angiotensin binding site in the mouse. Eur. J. Pharmacol., 590, 87-92.
106. Maul, B., von Bohlen und Halbach, O., Becker, A., Sterner-Kock, A., Voigt, J.-P., Siems, W.-E., Grecksch, G. and Walther, T. (2008). Impaired spatial memory and altered dendritic spine morphology in angiotensin II type 2 receptor-deficient mice. J. Mol. Med., 86, 563-71.
105. Sun, X., Becker, M., Pankow, K., Krause, E., Ringling, M., Beyermann, M., Maul, B., Walther, T., and Siems, W.-E. (2008).
104. Riad*, A., Walther*, T., Yang, J., Altmann, C., Escher, F., Westermann, D., Spillmann, F., Schultheiss, H.-P., and Tschöpe C. (2008). The cardiovascular influence of interleukin-1ß on the bradykinin B1 and B2 receptors. Internat. Immunopharmacol., 8, 222-30. *Equally contributing First authors.
103. Moreira, M.C., Heringer-Walther, S., Wessel, N., Moreira Ventura, T., Wang Y., Schultheiss, H.-P., and Walther, T. (2008). Prognostic value of natriuretic peptides in Chagas' disease: a 3-year follow-up investigation. Cardiology, 2008, 110, 217-225.
102. Pankow, K., Wang, Y., Gembardt, F., Krause, E., Sun, X., Krause, G., Schultheiss, H.-P., Siems, W.-E., and Walther, T. (2007). A successive action of meprin A and neprilysin catabolizes B-type natriuretic peptide. Circulation Res., 101, 875-82.
101. Peiro, C., Vallejo, S., Gembardt, F., Azcutia, V., Heringer-Walther, S., Rodriguez-Manas, L., Schultheiss, H.-P., Sanchez-Ferrer, C.F., and Walther, T. (2007). Endothelial dysfunction through genetic deletion or inhibition of the G protein-coupled receptor Mas - a new target to improve endothelial function. J. Hypertens., 25, 2421-2425.
100. Yousif, M.H.M., Akhtar, S., Walther, T., and Benter, I.F. (2007). Role of Ca2+/calmodulin-dependent protein kinase II in development of vascular dysfunction in diabetic rats with hypertension. Cell Biochem. Funct., in press.
99. Stepan, H. & Walther, T. (2007).
98. Becker, L.K., Etelvino, G.M., Walther, T., Santos, R.A.S., Campagnole-Santos, M.J. (2007). Immunofluorescence localization of the receptor Mas in cardiovascular-related areas of the rat brain. Am. J. Physiol. Heart Circ. Physiol., 293, H1416-24.
97. Wang, Y., de Waard, M.C., Sterner-Kock, A., Stepan, H., Schultheiss, H.-P., Duncker, D.J., and Walther, T. (2007).
96. Malberg, H., Bauernschmitt, R., Voss, A., Walther, T., Faber, R., Stepan, H., and Wessel, N. (2007).
95. Walther, T and Stepan, H. (2007).
94. Stepan, H., Wallukat, G., Schultheiss, H.-P., Faber, R., and Walther, T. (2007).
93. Wessel, N., Malberg, H., Heringer-Walther, S., Schultheiss, H.-P., and Walther, T. (2007). The angiotensin-(1-7) receptor agonist AVE0991 dominates the circadian rhythm and baroreflex in spontaneously hypertensive rats. J. Cardiovasc. Pharmacol., 49, 67-73.
92. Walther, T., Tschöpe, C., Sterner-Kock, A., Westermann, D., Heringer-Walther, S., Riad, A., Nikolic, A., Wang, Y., Ebermann, L., Siems, W.-E., Bader, M., Shakibaei, M., Schultheiss, H.-P., and Dörner, A. (2007).
91. Heringer-Walther, S., Moreira, M.C., Wessel, N., Wang, Y., Moreira Ventura, T., Schultheiss, H.-P., and Walther, T. (2006). Does the C-type natriuretic peptide have prognostic value in Chagas' disease and other dilated cardiomyopathies? J. Cardiovasc. Pharmacol., 48, 293-298.
90. Koch, M., Spillmann, F., Dendorfer, A., Westermann, D., Altmann, C., Sahabi, M. Van Linthout, S., Bader, M., Walther, T., Schultheiss, H.-P., and Tschöpe, C. (2006).
89. Faber, F., Gembardt, F., Sun, X., Mizutani, S., Siems, W.-E., and Walther, T. (2006). Lack of angiotensin II conversion to angiotensin III increases water but not alcohol consumption in aminopeptidase A-deficient mice. Regulatory Peptides, 136, 130-137.
88. Mehrotra, S., Zhang, J., Teunissen, A.W., Saxena, P.R., Vandenbrink, A.M., Walther, T., and Sharma, H.S. (2006). Cloning of the porcine ?2b adrenoceptor: Tissue distribution and pharmacological characterization. Eur. J. Pharmacol., 545, 115-122.
87. Stepan, H., Faber, R., Wessel, N., Wallukat, G., Schultheiss, H.-P., and Walther, T. (2006).
86. van Esch, J., Schuijt, P., Sayed, J., Choudhry, Y., Walther, T., and Danser, AJ. (2006). AT2 Receptor-Mediated Vasodilation in the Mouse Heart depends on AT1A Receptor Activation. Brit. J. Pharmacol., 148, 452-458.
85. Batenburg, W., van Esch, J., Garrelds, I., Jorde, U., Lamers, J., Dekkers, D., Walther, T., Kellett, E., Milligan, G., van Kats, J., and Danser, J. (
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