SERCA in genesis of arrhythmias: what we already know and what is new?

• Published in: Anadolu kardiyoloji dergisi : AKD Vol. 7 Suppl 1; no. 1; pp. 43 - 46
• Main Author: Erkasap, Nilüfer
• Format: Journal Article
• Language: English
• Published: Turkey KARE Publishing 01.07.2007
• Subjects: Arrhythmia; Arrhythmias, Cardiac - physiopathology; Calcium Signaling; Causes of; Health aspects; Humans; Sarcoplasmic reticulum; Sarcoplasmic Reticulum - enzymology; Sarcoplasmic Reticulum - metabolism; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism; Turkey
• ISSN: 1302-8723; 1308-0032

This review mainly focuses on the structure, function of the sarco(endo)plasmic reticulum calcium pump (SERCA) and its role in genesis of arrhythmias. SERCA is a membrane protein that belongs to the family of P-type ion translocating ATPases and pumps free cytosolic calcium into intracellular stores. Active transport of Ca2+ is achieved, according to the E1-E2 model, changing of SERCA structure by Ca2+. The affinity of Ca2+ -binding sites varies from high (E1) to low (E2). Three different SERCA genes were identified-SERCA1, SERCA2, and SERCA3. SERCA is mainly represented by the SERCA2a isoform in the heart. In heart muscle, during systole, depolarization triggers the release of Ca2+ from the sarcoplasmic reticulum (SR) and starts contraction. During diastole, muscle relaxation occurs as Ca2+ is again removed from cytosol, predominantly by accumulation into SR via the action of SERCA2a. The main regulator of SERCA2a is phospholamban and another regulator proteolipid of SERCA is sarcolipin. There are a lot of studies on the effect of decreased and/or increased SERCA activity in genesis of arrhythmia. Actually both decrease and increase of SERCA activity in the heart result in some pathological mechanisms such as heart failure and arrhythmia.