Protein trafficking abnormalities: a new mechanism in drug‐induced long QT syndrome
Key result
Pentamidine at near therapeutic concentrations disrupts normal KCNH2 channel protein processing and maturation, reducing its surface membrane expression as a novel mechanism for drug-induced LQTS.
Design
Editorial
Authors
Discussion
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Member takes
Implication
Highlights a novel mechanism for drug-induced long QT syndrome where pentamidine disrupts KCNH2 channel protein trafficking rather than directly blocking the channel.
Structured PICO
E
Exposure
Pentamidine
O
Outcome
KCNH2 channel protein processing and maturationsurrogate
Highlights a novel mechanism for drug-induced long QT syndrome where pentamidine disrupts KCNH2 channel protein trafficking rather than directly blocking the channel.
Cite This Study
Eckhardt et al. (2005) conducted an editorial in Drug-induced long QT syndrome (LQTS). Pentamidine was evaluated on KCNH2 channel protein processing and maturation. Pentamidine at near therapeutic concentrations disrupts normal KCNH2 channel protein processing and maturation, reducing its surface membrane expression as a novel mechanism for drug-induced LQTS.