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• W3141561812 startingPage "139" @default.
• W3141561812 abstract "The human ether-á-go-go related gene (hERG, KCNH2) encodes the pore-forming subunit of the potassium channel responsible for a fast component of the cardiac delayed rectifier potassium current (IKr). Outward IKr is an important determinant of cardiac action potential (AP) repolarization and effectively controls the duration of the QT interval in humans. Dysfunction of hERG channel can cause severe ventricular arrhythmias and thus modulators of the channel, including hERG inhibitors and activators, continue to attract intense pharmacological interest. Certain inhibitors of hERG channel prolong the action potential duration (APD) and effective refractory period (ERP) to suppress premature ventricular contraction and are used as class III antiarrhythmic agents. However, a reduction of the hERG/IKr current has been recognized as a predominant mechanism responsible for the drug-induced delayed repolarization known as acquired long QT syndromes (LQTS), which is linked to an increased risk for torsades de pointes (TdP) ventricular arrhythmias and sudden cardiac death. Many drugs of different classes and structures have been identified to carry TdP risk. Hence, assessing hERG/IKr blockade of new drug candidates is mandatory in the drug development process according to the regulatory agencies. In contrast, several hERG channel activators have been shown to enhance IKr and shorten the APD and thus might have potential antiarrhythmic effects against pathological LQTS. However, these activators may also be proarrhythmic due to excessive shortening of APD and the ERP." @default.
• W3141561812 created "2021-04-13" @default.
• W3141561812 creator A5028277578 @default.
• W3141561812 creator A5040224347 @default.
• W3141561812 creator A5052492909 @default.
• W3141561812 creator A5080918574 @default.
• W3141561812 date "2021-01-01" @default.
• W3141561812 modified "2023-10-18" @default.
• W3141561812 title "Cardiac hERG K+ Channel as Safety and Pharmacological Target" @default.
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