Calcium entry channels and their role in the pathogenesis of acute pancreatitis

Acute pancreatitis (AP) is a common gastrointestinal emergency, and dysregulated calcium (Ca 2+ ) homeostasis within pancreatic acinar cells plays a key role in its development via intracellular Ca 2+ toxicity and mitochondrial collapse. Abnormal activation of plasma membrane Ca 2+ entry channels—including store-operated calcium entry (SOCE) channels, transient receptor potential (TRP) channels, and the mechanosensitive channel Piezo1—causes sustained cytosolic calcium overload. This imbalance triggers a series of harmful events, including premature zymogen activation and mitochondrial dysfunction, that create a vicious cycle of cellular injury in the pancreas. Growing evidence highlights the vital role of these Ca 2+ entry channels in the pathophysiology of AP. Our review outlines current understanding of how these channels contribute to AP development and discusses recent advances, therapeutic applications, and future directions for drug strategies targeting these channels.