Impaired CaV1.2 inactivation reduces the efficacy of calcium channel blockers in the treatment of LQT8

Mutations in the CaV1.2  L-type calcium channel can cause a profound form of long-QT syndrome known as long-QT type 8 (LQT8), which results in cardiac arrhythmias that are often fatal in early childhood. A growing number of such pathogenic mutations in CaV1.2 have been identified, increasing the need for targeted therapi es. As many of these mutations reduce channel inactivation; resulting in excess Ca2+ entry during the action potential, calcium channel blockers (CCBs) would seem to represent a promising treatment option.

Source: Journal of Molecular and Cellular Cardiology - October 19, 2022 Category: Cytology Authors: Moradeke A. Bamgboye, Maria K. Traficante, Josiah Owoyemi, Deborah DiSilvestre, Daiana C.O. Vieira, Ivy E. Dick Source Type: research