Publications by authors named "Xiuming Dong"
Article Synopsis
- Inhibiting Nav1.7 channels is a potential method for creating new pain relief treatments, particularly utilizing peptide toxins from spider venom.
- A study found that different spider venom peptides effectively inhibited both hNav1.7 and certain potassium (rKv4.2/4.3) channels, but targeted design could improve selectivity for pain relief.
- The development of a modified peptide, mGpTx1-SA, showed strong pain relief with less effect on rKv4.2/4.3 and reduced heart toxicity, hinting at future advancements in safer analgesic drugs specifically targeting hNav1.7.
Background: Previous studies have associated slowed ventricular conduction with the arrhythmogenesis mediated by the gap junction and sodium channel inhibitor heptanol in mouse hearts. However, they did not study the propagation patterns that might contribute to the arrhythmic substrate. This study used a multi-electrode array mapping technique to further investigate different conduction abnormalities in Langendorff-perfused mouse hearts exposed to 0.
View Article and Find Full Text PDFThe human ether-a-go-go-related gene (hERG) encodes the K channel that carries the rapid component of the delayed rectifier current in the human heart. Reduction of hERG activity induced by gene mutations or pharmacological inhibition is responsible for the type 2 form of long QT syndrome in patients which can develop into ventricular arrhythmia and sudden cardiac death. Therefore, pharmacological activation of hERG may lead to therapeutic potential for cardiac arrhythmias.
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