M
Michael K. Schuhmann
Researcher at University of Würzburg
Publications - 82
Citations - 3231
Michael K. Schuhmann is an academic researcher from University of Würzburg. The author has contributed to research in topics: Stroke & Medicine. The author has an hindex of 24, co-authored 67 publications receiving 2377 citations. Previous affiliations of Michael K. Schuhmann include University of Münster.
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Journal ArticleDOI
Animal models of ischemic stroke and their application in clinical research.
TL;DR: These models differ from human stroke, which particularly affects elderly people who have various cerebrovascular risk factors and optimizing the study design of preclinical trials might increase the translational potential of animal stroke models.
Journal ArticleDOI
Post-stroke inhibition of induced NADPH oxidase type 4 prevents oxidative stress and neurodegeneration.
Christoph Kleinschnitz,Henrike Grund,Kirstin Wingler,Melanie E. Armitage,Emma S Jones,Manish Mittal,David Barit,Tobias Schwarz,Christian Geis,Peter Kraft,K. Barthel,Michael K. Schuhmann,Alexander M. Herrmann,Sven G. Meuth,Guido Stoll,Sabine Meurer,Anja Schrewe,Lore Becker,Valerie Gailus-Durner,Helmut Fuchs,Thomas Klopstock,Martin Hrabé de Angelis,Karin Jandeleit-Dahm,Ajay M. Shah,Norbert Weissmann,Harald H.H.W. Schmidt +25 more
TL;DR: The identification of NOx4 as a major source of oxidative stress in stroke and demonstration of dramatic protection after stroke in mice by NOX4 deletion or NOX inhibition, opens up new avenues for treatment.
Journal ArticleDOI
STIM2 Regulates Capacitive Ca2+ Entry in Neurons and Plays a Key Role in Hypoxic Neuronal Cell Death
Alejandro Berna-Erro,Attila Braun,Robert Kraft,Christoph Kleinschnitz,Michael K. Schuhmann,David Stegner,Thomas Wultsch,Jens Eilers,Sven G. Meuth,Guido Stoll,Bernhard Nieswandt +10 more
TL;DR: It is shown that STIM2, but not STIM1, is essential for CCE and ischemia-induced cytosolic Ca2+ accumulation in neurons, which implicate CCE in ischemic neuronal cell death and establishSTIM2 as a critical mediator of this process.
Journal ArticleDOI
FTY720 Ameliorates Acute Ischemic Stroke in Mice by Reducing Thrombo-Inflammation but Not by Direct Neuroprotection
Peter Kraft,Eva Göb,Michael K. Schuhmann,Kerstin Göbel,Carsten Deppermann,Ina Thielmann,Alexander M. Herrmann,Kristina Lorenz,Marc Brede,Guido Stoll,Sven G. Meuth,Bernhard Nieswandt,Waltraud Pfeilschifter,Christoph Kleinschnitz +13 more
TL;DR: Induction of lymphocytopenia and concomitant reduction of microvascular thrombosis are key modes of FTY720 action in stroke, and findings in Rag1−/− mice and cultured neurons argue against direct neuroprotective effects of F TY720.
Journal ArticleDOI
Endothelial TWIK-related potassium channel-1 (TREK1) regulates immune-cell trafficking into the CNS
Stefan Bittner,Tobias Ruck,Michael K. Schuhmann,Michael K. Schuhmann,Alexander M. Herrmann,Hamid Moha Ou Maati,Nicole Bobak,Kerstin Göbel,Friederike Langhauser,David Stegner,Petra Ehling,Marc Borsotto,Hans-Christian Pape,Bernhard Nieswandt,Christoph Kleinschnitz,Catherine Heurteaux,Hans-Joachim Galla,Thomas Budde,Heinz Wiendl,Sven G. Meuth +19 more
TL;DR: Altered mitogen-activated protein (MAP) kinase signaling, actin remodeling and upregulation of cellular adhesion molecules as potential mechanisms of increased migration in TREK1-deficient mice suggest TREK-1 activating compounds may be used therapeutically to treat diseases related to BBB dysfunction.