Yvonne Reinke

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In cardiovascular diseases, reduced responsiveness of soluble guanylate cyclase (sGC) to nitric oxide (NO) upon long-term application has led to the development of NO-independent sGC stimulators (heme-dependent) and sGC activators (heme-independent). Any direct inotropic or lusitropic effects of these compounds on isolated cardiac myocytes, however, remain(More)
BACKGROUND Autoantibodies against β1-adrenergic receptors (β1AR) that stimulate cardiac cAMP-production play a causal role in the pathogenesis of human heart failure. Patients can be subjected to specific therapies, if the presence of potentially cardio-noxious β1AR-autoantibodies is reliably diagnosed. This requires assessment of IgG-interactions with the(More)
Auto-antibodies against cardiac proteins have been described in patients with dilated cardiomyopathy. Antibodies against the C-terminal part of KChIP2 (anti-KChIP2 [C-12]) enhance cell death of rat cardiomyocytes. The underlying mechanisms are not fully understood. Therefore, we wanted to explore the mechanisms responsible for anti-KChIP2-mediated cell(More)
In the clinical setting, administration of organic nitrates and nitric oxide (NO) donors has serious limitations such as resistance to NO and organic nitrates due to insufficient biometabolism and development of tolerance following prolonged administration of NO soluble guanylate cyclase (sGC) to NO [1,2]. This circumstance has led to development of(More)
Immunoadsorption with subsequent immunoglobulin substitution (IA/IgG) represents a therapeutic approach for patients with dilated cardiomyopathy (DCM). Here, we studied which molecular cardiac alterations are initiated after this treatment. Transcription profiling of endomyocardial biopsies with Affymetrix whole genome arrays was performed on 33 paired(More)
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