Therapeutic SERCA Enhancement – why and how
Cardiac Bioelectricity & Arrhythmia Center (CBAC), Washington University in St. Louis
Prof. Antonio Zaza
Tuesday, September 28, 2021
Virtual Seminar - 17:00 Rome Time / 10:00 am US Central Time
For the Zoom link, register here
more information: LINK
Abstract: SERCA2a is an ATPase transporter primarily responsible of Ca2+ confinement in the sarcoplasmic reticulum (SR) of cardiac myocytes. SERCA2a function, pivotal in the excitation-contraction coupling, is also relevant to cellular electrophysiology, because it affects the stability of SR as a Ca2+ store. SERCA2a downregulation plays an important role in the susceptibility to arrhythmias peculiar of heart failure. Therefore, in the failing heart, therapeutic SERCA2a enhancement may be desirable to restore electrical stability, as well as mechanical function. On the other hand, SR Ca2+ overload may compromise store stability, with a proarrhythmic effect; therefore, SERCA2a enhancement may be seen as “a double-edged” tool. The seminar will discuss the rationale of SERCA2a enhancement, novel pharmacological tools by which it can be achieved and their application to the treatment of a genetic form of heart failure, primarily associated with abnormality of SERCA2a regulatome.
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