A protein-degradation mechanism opens a new treatment route for an inherited arrhythmia

by Centro Nacional de Investigaciones Cardiovasculares

edited by Gaby Clark , reviewed by Andrew Zinin

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Add as preferred source The R33Q mutation in calsequestrin 2 (CASQ2) disrupts calcium control in heart cells and activates protein-degradation mechanisms. Credit: CNIC An international team has identified a protein-degradation mechanism that contributes to the development of an inherited form of catecholaminergic polymorphic ventricular tachycardia (CPVT), a disease that mainly affects children and young people. The study was led by researchers at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), in collaboration with the University of Pavia and IRCCS Istituti Clinici Scientifici Maugeri in Italy.