Receptor-mediated calcium entry (RMCE) (RMCE)

Receptor-mediated calcium entry (RMCE) in platelets is a fundamental signaling mechanism that regulates the elevation of cytosolic calcium levels necessary for platelet activation and thrombus formation (Varga-Szabo et al., 2009). This process involves two main pathways: store-operated calcium entry (SOCE), which is activated by the depletion of internal calcium stores and mediated by the STIM1 sensor and Orai1 channel, and receptor-operated calcium entry (ROCE), which occurs through ionotropic receptors like P2X1 or TRP channels (Bergmeier & Stefanini, 2013). Upon vascular injury, agonists such as thrombin and ADP trigger these pathways to facilitate shape change, granule secretion, and the activation of integrin alpha-IIb/beta-3 (Heemskerk et al., 2002). While essential for normal hemostasis, dysregulated RMCE contributes to the development of arterial thrombosis, leading to conditions such as myocardial infarction and stroke (Braun et al., 2009). Pharmacological modulation of RMCE components, such as Orai1 or P2X1, represents a promising strategy for antiplatelet therapy, aiming to inhibit pathological clot formation while preserving some level of hemostatic function.

Other names

ROCESOCEStore-operated calcium entryReceptor-operated calcium entryReceptor-mediated Ca2+ entry

Inhibition of calcium influx through plasma membrane channels (such as Orai1 or P2X1) to prevent the rise in cytosolic calcium required for platelet activation and aggregation.