Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis

doi:10.3748/wjg.v20.i43.16146

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World Journal of Gastroenterology

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1007-9327

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World J Gastroenterol. Nov 21, 2014; 20(43): 16146-16152
Published online Nov 21, 2014. doi: 10.3748/wjg.v20.i43.16146

Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis

Jun Li, Rui Zhou, Jian Zhang, Zong-Fang Li

Jun Li, National Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, the Second Affiliated Hospital of Xi’an Jiaotong University College of Medicine, Xi’an 710004, Shaanxi Province, China

Rui Zhou, Jian Zhang, Zong-Fang Li, Department of General Surgery, National Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, the Second Affiliated Hospital of Xi’an Jiaotong University College of Medicine, Xi’an 710004, Shaanxi Province, China

Author contributions: Li J and Zhou R collected the underlying material and wrote the initial draft of the manuscript; Li J, Zhou R, Zhang J and Li ZF designed the outline of the paper; Li ZF finalized and revised the manuscript; all authors read and approved the final version of the manuscript.

Supported by grants from the National Natural Science Foundation of China No. 30171167, No. 30901945 and the Specialized Research Fund for the Doctoral Program of Higher Education No. 20130201130009

Correspondence to: Zong-Fang Li, MD, PhD, Department of General Surgery, National Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi’an Jiaotong University College of Medicine, No. 157 West 5^th Road, Xi’an 710004, Shaanxi Province, China. lzf2568@gmail.com

Telephone: +86-29-87678006 Fax: +86-29-87678634

Received: February 28, 2014
Revised: June 9, 2014
Accepted: July 11, 2014
Published online: November 21, 2014
Processing time: 265 Days and 9.1 Hours

Core Tip

Core tip: Calcium (Ca²⁺) overload is crucial in the pathogenesis of pancreatitis, which results in trypsin activation, vacuolization and necrosis. Such cell injury results from increased Ca²⁺ released from intracellular endoplasmic reticulum Ca²⁺ stores, increased Ca²⁺ entry through the plasma membrane and Ca²⁺ pump defects. Current findings have provided further insight into the roles and mechanisms of Ca²⁺ overload in pancreatitis. The lack of specific treatments is a stimulus for ongoing research. This review summarizes recent advances in our understanding of Ca²⁺ signaling in the pathogenesis of pancreatitis, and discusses how research has guided our search for potential therapeutic targets.