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.