CNIC researchers identify enzyme inhibition to reduce ventricular arrhythmias

An international research team led by the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) has identified a protein degradation mechanism involved in catecholaminergic polymorphic ventricular tachycardia (CPVT). This hereditary arrhythmia primarily affects children and young adults, often triggered by exercise or emotional stress, and can lead to sudden death.

The study, published in Circulation Research, focused on a form of CPVT caused by a mutation in the gene encoding calsequestrin, a protein responsible for regulating calcium within heart cells. Researchers found that inhibiting the enzyme calpain reduced the occurrence of ventricular arrhythmias in experimental mouse models by restoring essential proteins required for calcium regulation.

The research was conducted in collaboration with the University of Pavia and the Irccs Istituti Clinici Scientifici Maugeri in Italy, as well as the Cardiovascular Disease Biomedical Research Network (Cibercv).