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447 results on '"Steinhoff, Gustav"'

10. Safety of Simultaneous Coronary Artery Bypass Grafting and Carotid Endarterectomy Versus Isolated Coronary Artery Bypass Grafting: A Randomized Clinical Trial

Author

Weimar, Christian, Bilbilis, Konstantinos, Rekowski, Jan, Holst, Torulv, Beyersdorf, Friedhelm, Breuer, Martin, Dahm, Manfred, Diegeler, Anno, Kowalski, Arne, Martens, Sven, Mohr, Friedrich W., Ondrášek, Jiri, Reiter, Beate, Roth, Peter, Seipelt, Ralf, Siggelkow, Markus, Steinhoff, Gustav, Moritz, Anton, Wilhelmi, Mathias, Wimmer-Greinecker, Gerhard, Diener, Hans-Christoph, Jakob, Heinz, Ose, Claudia, Scherag, Andre, and Knipp, Stephan C.

Published
2017
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17. The regenerative potential of angiotensin [AT.sub.2] receptor in cardiac repair

Author

Ludwig, Marion, Steinhoff, Gustav, and Li, Jun

Subjects
Regeneration (Biology) -- Physiological aspects -- Health aspects, Heart -- Physiological aspects -- Health aspects, Angiotensin -- Physiological aspects -- Health aspects, Biological sciences
Abstract

Angiotensin II, the main effector peptide of the renin-angiotensin system, interferes with cardiac remodeling and repair through its receptors, including [AT.sub.1] and [AT.sub.2] receptor (R). The functional relevance of the previously neglected [AT.sub.2]R is currently intensively studied. Pharmacological therapies with [AT.sub.1]R blockers have improved outcomes in patients with ischemic heart injury, probably involving an indirect stimulation of [AT.sub.2]R. Previous experimental studies have clearly shown a protective action of [AT.sub.2]R in tissue repair and regeneration. We have recently identified the [c- kit.sup.+][AT.sub.2][R.sup.+] progenitor cell population in rat heart and bone marrow, which increases after induction of myocardial infarction. Further experimental evidence demonstrates that [AT.sub.2]R mediates cardiac homing and repair process of the [c-kit.sup.+] progenitor cells. [AT.sub.2]R stimulation through [AT.sub.1]R blockers or directly by [AT.sub.2]R agonist or both in combination may potentially offer the translational options to improve the regenerative potentials of stem/progenitor cells derived from patients with cardiovascular disease. Key words: angiotensin, AT2 receptor, progenitor cell, cardiac repair, regeneration. L'angiotensine II, le principal peptide effecteur du systeme renine-angiotensine, interfere avec le remodelage et la reparation cardiaques par l'intermediaire de ses recepteurs (R) [AT.sub.1] et [AT.sub.2]. La pertinence fonctionnelle du [RAT.sub.2], autrefois negligee, fait actuellement l'objet d'etudes intensives. Les therapies pharmacologiques utilisant les bloqueurs du [RAT.sub.1] ont ameliore le pronostic des patients presentant une maladie cardiaque ischemique, probablement par une stimulation indirecte du [RAT.sub.2]. Des etudes experimentales anterieures ont clairement montre une action protectrice du [RAT.sub.2] dans la reparation et la regeneration des tissus. Recemment, nous avons identifie la population de cellules progenitrices [c- kit.sup.+][RAT.sub.2] dans le creur et la moelle osseuse des rats, laquelle augmente apres un infarctus du myocarde. D'autres resultats experimentaux demontrent que le [RAT.sub.2] medie le processus de reparation et de migration cardiaques des cellules progenitrices [c- kit.sup.+]. La stimulation du [RAT.sub.2] par l'intermediaire des bloqueurs du [RAT.sub.1], ou directement par un agoniste du [RAT.sub.2], ou par une combinaison des deux sources pourrait offrir les options translationnelles pour l'amelioration des potentiels regenerateurs des cellules souches/progenitrices provenant de patients atteints d'une maladie cardiovasculaire. Mots-cles : angiotensine, recepteur [AT.sub.2], cellules progenitrices, reparation cardiaque, regeneration. [Traduit par la Redaction], Introduction The interruption of blood supply to a part of the heart is mostly due to an occlusion of a coronary artery by a ruptured atherosclerotic plaque. Acute myocardial infarction [...]

Published
2012
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22. The Effects of Hypoxic Preconditioned Murine Mesenchymal Stem Cells on Post-Infarct Arrhythmias in the Mouse Model.

Author

Ahmad, Beschan, Skorska, Anna, Wolfien, Markus, Sadraddin, Haval, Lemcke, Heiko, Vasudevan, Praveen, Wolkenhauer, Olaf, Steinhoff, Gustav, David, Robert, and Gaebel, Ralf

Subjects
MESENCHYMAL stem cells, ARRHYTHMIA, MYOCARDIAL infarction, BRUGADA syndrome, LABORATORY mice, CARDIAC arrest, HEART failure, ANIMAL disease models
Abstract

Ventricular arrhythmias associated with myocardial infarction (MI) have a significant impact on mortality in patients following heart attack. Therefore, targeted reduction of arrhythmia represents a therapeutic approach for the prevention and treatment of severe events after infarction. Recent research transplanting mesenchymal stem cells (MSC) showed their potential in MI therapy. Our study aimed to investigate the effects of MSC injection on post-infarction arrhythmia. We used our murine double infarction model, which we previously established, to more closely mimic the clinical situation and intramyocardially injected hypoxic pre-conditioned murine MSC to the infarction border. Thereafter, various types of arrhythmias were recorded and analyzed. We observed a homogenous distribution of all types of arrhythmias after the first infarction, without any significant differences between the groups. Yet, MSC therapy after double infarction led to a highly significant reduction in simple and complex arrhythmias. Moreover, RNA-sequencing of samples from stem cell treated mice after re-infarction demonstrated a significant decline in most arrhythmias with reduced inflammatory pathways. Additionally, following stem-cell therapy we found numerous highly expressed genes to be either linked to lowering the risk of heart failure, cardiomyopathy or sudden cardiac death. Moreover, genes known to be associated with arrhythmogenesis and key mutations underlying arrhythmias were downregulated. In summary, our stem-cell therapy led to a reduction in cardiac arrhythmias after MI and showed a downregulation of already established inflammatory pathways. Furthermore, our study reveals gene regulation pathways that have a potentially direct influence on arrhythmogenesis after myocardial infarction. [ABSTRACT FROM AUTHOR]

Published
2022
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24. Gene delivery to the heart by magnetic nanobeads

Author

Li, Wenzhong, Nesselmann, Catharina, Zhou, Zhaohui, Ong, Lee-Lee, Öri, Ferenc, Tang, Guping, Kaminski, Alexander, Lützow, Karola, Lendlein, Andreas, Liebold, Andreas, Stamm, Christof, Wang, John, Steinhoff, Gustav, and Ma, Nan

Published
2007
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47. Mesenchymal stem cells and cardiac repair

Author

Nesselmann, Catharina, Ma, Nan, Bieback, Karen, Wagner, Wolfgang, Ho, Anthony, Konttinen, Yrjö T., Zhang, Hao, Hinescu, Mihail E., and Steinhoff, Gustav

Published
2008

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