Caspofungin modulates ryanodine receptor-mediated calcium release in human cardiac myocytes
Recent studies showed that critically ill patients might be at risk for hemodynamic impairment during caspofungin (CAS) therapy. The aim of our present study was to examine the mechanisms behind CAS-induced cardiac alterations. We revealed a dose-dependent increase in intracellular Ca2+ concentratio...
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| Hauptverfasser: | , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
October 24, 2018
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| In: |
Antimicrobial agents and chemotherapy
Year: 2018, Jahrgang: 62, Heft: 11 |
| ISSN: | 1098-6596 |
| DOI: | 10.1128/AAC.01114-18 |
| Online-Zugang: | Resolving-System, Volltext: https://doi.org/10.1128/AAC.01114-18 Verlag: https://aac.asm.org/content/62/11/e01114-18 
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| Verfasserangaben: | Christian Koch, Jennifer Jersch, Emmanuel Schneck, Fabian Edinger, Hagen Maxeiner, Florian Uhle, Markus A. Weigand, Melanie Markmann, Michael Sander, Michael Henrich |
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| 520 | |a Recent studies showed that critically ill patients might be at risk for hemodynamic impairment during caspofungin (CAS) therapy. The aim of our present study was to examine the mechanisms behind CAS-induced cardiac alterations. We revealed a dose-dependent increase in intracellular Ca2+ concentration ([Ca2+]i) after CAS treatment. Ca2+ ions were found to be released from intracellular caffeine-sensitive stores, most probably via the activation of ryanodine receptors. | ||
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