Enhanced store-operated calcium entry in platelets is associated with acute coronary syndrome

Enhanced store-operated calcium entry in platelets is associated with acute coronary syndrome: Acute coronary syndrome (ACS) is associated with sudden, reduced blood flow to the heart and usually correlated with coronary thrombosis [1]. Therefore, platelets play an important part in the pathogenesis and complications of ACS. Platelet activation is a complex event involving activation of intracellular signaling cascades, such as calcium signaling, which leads to platelet activation, secretion and aggregation. Platelets are highly specialized secretory cells that have a well characterized pattern of cell activation and intracellular signaling. Platelet activation causes increased cytosolic Ca²⁺ concentration, which could be limited by accelerating sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA) activity [2]. SERCA activity can be regulated by Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) [3]. Furthermore, it has been shown that CaMKII is increased in activated platelets, indicating that cytosolic Ca²⁺ concentration is crucial to induce platelet activation [4].