C
Christoph Maack
Researcher at University of Würzburg
Publications - 190
Citations - 11232
Christoph Maack is an academic researcher from University of Würzburg. The author has contributed to research in topics: Heart failure & Mitochondrion. The author has an hindex of 49, co-authored 161 publications receiving 8828 citations. Previous affiliations of Christoph Maack include Saarland University & University of Mainz.
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Journal ArticleDOI
2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism
Stavros Konstantinides,Stavros Konstantinides,Adam Torbicki,Giancarlo Agnelli,Nicolas Danchin,David Fitzmaurice,Nazzareno Galiè,J. Simon R. Gibbs,Menno V. Huisman,Marc Humbert,Nils Kucher,Irene Lang,Mareike Lankeit,John Lekakis,Christoph Maack,Eckhard Mayer,Nicolas Meneveau,Arnaud Perrier,Piotr Pruszczyk,Lars Hvilsted Rasmussen,Thomas H. Schindler,Pavel Svitil,Anton Vonk Noordegraaf,José Luis Zamorano,Maurizio Zompatori +24 more
TL;DR: This list of World War Two veterans includes those who fought in the theatres, on the battlefields, during the conflict and after, as well as those involved in the aftermath of the conflict.
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Oxygen Free Radical Release in Human Failing Myocardium Is Associated With Increased Activity of Rac1-GTPase and Represents a Target for Statin Treatment
Christoph Maack,Tanja Kartes,Heiko Kilter,Hans-Joachim Schäfers,Georg Nickenig,Michael Böhm,Ulrich Laufs +6 more
TL;DR: Failing myocardium of patients with DCM and ICM is characterized by upregulation of NADPH oxidase–mediated ROS release associated with increased rac1 activity, which suggests that extrahepatic effects of statins can be observed in humans and may be beneficial for patients with chronic heart failure.
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Metabolic remodelling in heart failure
Edoardo Bertero,Christoph Maack +1 more
TL;DR: It is suggested that the alterations of intermediate substrate metabolism and oxidative stress rather than an ATP deficit per se account for maladaptive cardiac remodelling and dysfunction under resting conditions.
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Elevated Cytosolic Na+ Decreases Mitochondrial Ca2+ Uptake During Excitation-Contraction Coupling and Impairs Energetic Adaptation in Cardiac Myocytes
TL;DR: The results indicate that mitochondria take up Ca2+ rapidly and contribute to fast buffering during a [Ca2+]c transient; and elevated Na+ ([Na+]i) impairs mitochondrial Ca2- uptake, with consequent effects on energy supply and demand matching.
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Calcium Signaling and Reactive Oxygen Species in Mitochondria
Edoardo Bertero,Christoph Maack +1 more
TL;DR: Targeting the dysregulated interplay between excitation–contraction coupling and mitochondrial energetics may ameliorate the progression of heart failure.