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 Ca concentration...

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Published inAntimicrobial agents and chemotherapy Vol. 62; no. 11
Main Authors Koch, Christian, Jersch, Jennifer, Schneck, Emmanuel, Edinger, Fabian, Maxeiner, Hagen, Uhle, Florian, Weigand, Markus A, Markmann, Melanie, Sander, Michael, Henrich, Michael
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.11.2018
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Summary: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 Ca concentration ([Ca ] ) after CAS treatment. Ca ions were found to be released from intracellular caffeine-sensitive stores, most probably via the activation of ryanodine receptors.
Bibliography:Citation Koch C, Jersch J, Schneck E, Edinger F, Maxeiner H, Uhle F, Weigand MA, Markmann M, Sander M, Henrich M. 2018. Caspofungin modulates ryanodine receptor-mediated calcium release in human cardiac myocytes. Antimicrob Agents Chemother 62:e01114-18. https://doi.org/10.1128/AAC.01114-18.
ISSN:0066-4804
1098-6596
DOI:10.1128/AAC.01114-18