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

Liao, Die, Li, Zhuoya, Sun, Zelin, Jia, Yao, He, Xuebiao, Yang, Xiaolin and Peng, Shuang 2025. Calcium entry channels and their role in the pathogenesis of acute pancreatitis. Cell Investigation , 100050. 10.1016/j.clnves.2025.100050

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Abstract

Acute pancreatitis (AP) is a common gastrointestinal emergency, and dysregulated calcium (Ca2+) homeostasis within pancreatic acinar cells plays a key role in its development via intracellular Ca2+ toxicity and mitochondrial collapse. Abnormal activation of plasma membrane Ca2+ 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 Ca2+ 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.

Item Type:	Article
Date Type:	Published Online
Status:	In Press
Schools:	Schools > Biosciences
Additional Information:	License information from Publisher: LICENSE 1: URL: http://creativecommons.org/licenses/by/4.0/, Start Date: 2025-11-12
Publisher:	Elsevier
ISSN:	3050-5380
Date of First Compliant Deposit:	25 November 2025
Date of Acceptance:	12 November 2025
Last Modified:	25 Nov 2025 11:30
URI:	https://orca.cardiff.ac.uk/id/eprint/182633

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