T
Thomas Boettger
Researcher at Max Planck Society
Publications - 77
Citations - 6859
Thomas Boettger is an academic researcher from Max Planck Society. The author has contributed to research in topics: Regulation of gene expression & Myocyte. The author has an hindex of 33, co-authored 70 publications receiving 5905 citations. Previous affiliations of Thomas Boettger include Lund University & University of Hamburg.
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Journal ArticleDOI
Atheroprotective communication between endothelial cells and smooth muscle cells through miRNAs.
Eduard Hergenreider,Susanne Heydt,Karine Tréguer,Thomas Boettger,Anton J.G. Horrevoets,Andreas M. Zeiher,Margot P. Scheffer,Achilleas S. Frangakis,Xiaoke Yin,Manuel Mayr,Thomas Braun,Carmen Urbich,Reinier A. Boon,Stefanie Dimmeler +13 more
TL;DR: The results show that atheroprotective stimuli induce communication between endothelial cells and SMCs through an miRNA- and extracellular-vesicle-mediated mechanism and that this may comprise a promising strategy to combat atherosclerosis.
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Acquisition of the contractile phenotype by murine arterial smooth muscle cells depends on the Mir143/145 gene cluster
Thomas Boettger,Nadine Beetz,Sawa Kostin,Johanna Schneider,Marcus Krüger,Lutz Hein,Thomas Braun +6 more
TL;DR: It is demonstrated that the mouse miR-143/145 cluster, expression of which is confined to SMCs during development, is required for VSMC acquisition of the contractile phenotype and manipulated expression may offer a new approach for influencing vascular repair and attenuating arteriosclerosis pathogenesis.
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Sirt7 Increases Stress Resistance of Cardiomyocytes and Prevents Apoptosis and Inflammatory Cardiomyopathy in Mice
Olesya Vakhrusheva,Christian Smolka,Praveen Gajawada,Sawa Kostin,Thomas Boettger,Thomas Kubin,Thomas Braun,Eva Bober +7 more
TL;DR: It is proposed that enhanced activation of p53 by lack of Sirt7-mediated deacetylation contributes to the heart phenotype of SIRT7 mutant mice, suggesting a critical role of Sirts in the regulation of stress responses and cell death in the heart.
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Barttin is a Cl- channel beta-subunit crucial for renal Cl- reabsorption and inner ear K+ secretion.
Raúl Estévez,Thomas Boettger,Valentin Stein,Ralf Birkenhäger,Edgar A. Otto,Friedhelm Hildebrandt,Thomas J. Jentsch +6 more
TL;DR: This work describes the first known β-subunit for CLC chloride channels and reveals that heteromers formed by ClC-K and barttin are crucial for renal salt reabsorption and potassium recycling in the inner ear.
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FOXO1 couples metabolic activity and growth state in the vascular endothelium.
Kerstin Wilhelm,Katharina Happel,Guy Eelen,Sandra Schoors,Mark F. Oellerich,Radiance Lim,Barbara Zimmermann,Irene M. Aspalter,Claudio A. Franco,Thomas Boettger,Thomas Braun,Marcus Fruttiger,Klaus Rajewsky,Charles Keller,Jens C. Brüning,Holger Gerhardt,Peter Carmeliet,Michael Potente,Michael Potente +18 more
TL;DR: It is reported that the forkhead box O (FOXO) transcription factor FOXO1 is an essential regulator of vascular growth that couples metabolic and proliferative activities in ECs and the FOXO–MYC transcriptional network is defined as a novel metabolic checkpoint during endothelial growth and proliferation.