Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis

Figure 1 Diagram showing possible interventions for therapeutic targets of pancreatitis. Blockage of Ca²⁺ entry will probably depend on inhibition of the store-operated Ca²⁺ (SOC) channel in the pancreatic acinar cell. Activation of plasma membrane Ca²⁺-adenosine triphosphate (ATP)ase (PMCA) and sarco/endoplasmic reticulum Ca²⁺-activated ATPase (SERCA) would enhance Ca²⁺ extrusion from the cell and endoplasmic reticulum (ER). Intracellular Ca²⁺ release from the ER can be prevented through inhibition of the inositol 1,4,5-trisphosphate receptor (IP₃R) and ryanodine receptor (RyR). Preconditioning strategies could protect mitochondrial function to ensure adequate ATP production extrusion by Ca²⁺ pumps and for pancreatic acinar cells to survive intact.