Local TH action in acute and chronic ischaemic heart disease

Prof. Dr. med. PhD Dagmar Führer,  Prof. Dr. med. Lars C. Möller  &  Prof. Dr. Kristina Lorenz

This project pursues the hypothesis that targeted TH action can be applied to reduce injury in acute myocardial infarction (MI) and to ameliorate post-MI remodelling. Using cell-specific mouse models, we will comprehensively characterise local control of TH action in acute and chronic ischaemic heart disease (IHD) and in these conditions will dissect the role of TR isoform, and the mode of TR action in endothelial cells and cardiomyocytes. Furthermore, we will define the optimal timing for TH intervention and will explore selective targeting. Our long-term goal is to exploit local TH action for the benefit of patients with IHD.


Project Team Members

Susanne Grund Postdoc (Team Führer, Möller) +49 201 723 4376 This email address is being protected from spambots. You need JavaScript enabled to view it.
Yara Maria Machlah Clinician Scientist (Team Führer, Möller)   This email address is being protected from spambots. You need JavaScript enabled to view it.
Dr. rer. nat. Christina Wenzek Postdoc (Team Führer) +49 201 723 83254 This email address is being protected from spambots. You need JavaScript enabled to view it.
Ann-Kathrin Schörding MD candidate (Team Möller)    
Stefanie Dörr PhD candidate (Team Lorenz) +49 231 13 92 289 Mail
Edeltraut Hoffmann-Posorske Lab Technician (Team Lorenz) +49 231 1392 243 This email address is being protected from spambots. You need JavaScript enabled to view it.
Konstanze Schättel Lab Technician (Team Lorenz) +49 201 723 82527 This email address is being protected from spambots. You need JavaScript enabled to view it.

Further Information

Homepage Team Führer

Homepage Team Möller

Homepage Team Lorenz


Selected Publications

Noncanonical Action of Thyroid Hormone Receptors α and β.
Hönes GS, Geist D, Moeller LC.
2020. Exp Clin Endocrinol Diabetes 128(6-07):383-387. doi: 10.1055/a-1088-1187

Increased Anaplastic Lymphoma Kinase Activity Induces a Poorly Differentiated Thyroid Carcinoma in Mice.
Kohler H, Latteyer S, Hönes GS, Theurer S, Liao XH, Christoph S, Zwanziger D, Schulte JH, Kero J, Undeutsch H, Refetoff S, Schmid KW, Führer DMoeller LC.
2019. Thyroid 29(10):1438-1446. doi: 10.1089/thy.2018.0526

Thyroxine promotes lung cancer growth in an orthotopic mouse model.
Latteyer S, Christoph S, Theurer S, Hönes GS, Schmid KW, Führer DMoeller LC.
2019. Endocr Relat Cancer 26(6):565-574. doi: 10.1530/ERC-18-0353

Noncanonical thyroid hormone signaling mediates cardiometabolic effects in vivo.
Hönes GS, Rakov H, Logan J, Liao XH, Werbenko E, Pollard AS, Præstholm SM, Siersbæk MS, Rijntjes E, Gassen J, Latteyer S, Engels K, Strucksberg KH, Kleinbongard P, Zwanziger D, Rozman J, Gailus-Durner V, Fuchs H, Hrabě de Angelis M, Klein-Hitpass L, Köhrle J, Armstrong DL, Grøntved L, Bassett JHD, Williams GR, Refetoff S, Führer DMoeller LC.
2017. Proc Natl Acad Sci U S A 26;114(52):E11323-E11332. doi: 10.1073/pnas.1706801115

A 6-Base Pair in Frame Germline Deletion in Exon 7 Of RET Leads to Increased RET Phosphorylation, ERK Activation, and MEN2A.
Latteyer S, Klein-Hitpass L, Khandanpour C, Zwanziger D, Poeppel TD, Schmid KW, Führer DMoeller LC.
2016. J Clin Endocrinol Metab 101(3):1016-22. doi: 10.1210/jc.2015-2948

A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy.
Lorenz K, Schmitt JP, Schmitteckert EM, Lohse MJ.
2009. Nat Med 15(1):75-83. doi: 10.1038/nm.1893

Interference with ERK-dimerization at the nucleocytosolic interface targets pathological ERK1/2 signaling without cardiotoxic side-effects.
Tomasovic T, Brand T, Schanbacher C, Kramer S, Hümmert MW, Godoy P, Schmidt-Heck W, Nordbeck P, Ludwig J, Homann S, Wiegering A, Shaykhutdinov T, Kratz C, Knüchel R, Müller-Hermelink HK, Rosenwald A, Frey N, Eichler J, Dobrev D, El-Armouche A, Hengstler JG, Müller OJ, Hinrichs K, Cuello F, Zernecke A, Lorenz K.
2020. Nat Commun 11, 1733. doi: 10.1038/s41467-020-15505-4

Phosphodiesterase 2 Protects Against Catecholamine-Induced Arrhythmia and Preserves Contractile Function After Myocardial Infarction.
Vettel C, Lindner M, Dewenter M, Lorenz K, Schanbacher C, Riedel M, Lämmle S, Meinecke S, Mason FE, Sossalla S, Geerts A, Hoffmann M, Wunder F, Brunner FJ, Wieland T, Mehel H, Karam S, Lechêne P, Leroy J, Vandecasteele G, Wagner M, Fischmeister R, El-Armouche A.
2017. Circ Res 120(1):120-132. doi: 10.1161/CIRCRESAHA.116.310069

Interference with ERKThr188-phosphorylation impairs pathological but not physiological cardiac hypertrophy.
Ruppert C, Deiss K, Herrmann S, Vidal M, Oezkur M, Gorski A, Weidemann F, Lohse MJ, Lorenz K.
2013. Proc Natl Acad Sci U S A 110(18):7440-5. doi: 10.1073/pnas.1221999110

Cardiac RKIP causes a beneficial beta-adrenoceptor-dependent positive inotropy.
Schmid E, Neef S, Berlin C, Tomasovic A, Kahlert K, Nordbeck P, Deiss K, Denzinger S, Herrmann S, Wettwer E, Weidendorfer M, Becker D, Schäfer F, Wagner N, Ergün S, Schmitt JP, Katus HA, Weidemann F, Ravens U, Maack C, Hein L, Ertl G, Müller OJ, Maier LS, Lohse MJ, Lorenz K.
2015. Nat Med 21(11):1298-306. doi: 10.1038/nm.3972