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12/5/2014 11:43:00 AM | Browse: 916 | Download: 1077
Publication Name World Journal of Gastroenterology
Manuscript ID 9804
Country China
Received
2014-03-01 12:16
Peer-Review Started
2014-03-01 18:52
To Make the First Decision
2014-05-13 20:29
Return for Revision
2014-05-21 08:51
Revised
2014-06-09 00:00
Second Decision
2014-07-11 17:02
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2014-07-11 17:17
Articles in Press
2014-07-11 17:34
Publication Fee Transferred
Edit the Manuscript by Language Editor
2014-07-19 20:21
Typeset the Manuscript
2014-11-11 10:24
Publish the Manuscript Online
2014-11-20 20:51
ISSN 1007-9327 (print) and 2219-2840 (online)
Open Access
Copyright
Article Reprints For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
Permissions For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
Publisher Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Website http://www.wjgnet.com
Category Surgery
Manuscript Type Topic Highlights
Article Title Calcium signalling of pancreatic acinar cells in the pathogenesis of pancreatitis
Manuscript Source Invited Manuscript
All Author List Jun Li, Rui Zhou, Jian Zhang and Zong-Fang Li
Funding Agency and Grant Number
Funding Agency Grant Number
National Natural Science Foundation of China 30171167
National Natural Science Foundation of China 30901945
Specialized Research Fund for the Doctoral Program of Higher Education 20130201130009
Corresponding Author Zong-Fang Li, MD, PhD, National Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, Department of General Surgery, the Second Affiliated Hospital of Xi’an Jiaotong University College of Medicine, No. 157 West 5th Road, Xi'an 710004, Shaanxi Province, China. lzf2568@gmail.com
Key Words Pancreatitis; Calcium signaling; Pancreatic acinar cells; Overload; Cell injury
Core Tip 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 absence of specific treatments is a spur to research. This review summarize recent advances in our understanding of Ca2+ signalling in the pathogenesis of pancreatitis, and discuss how research has guided our search for potential therapeutic targets.
Publish Date 2014-11-20 20:51
Citation Li J, Zhou R, Zhang J, Li ZF. Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis. World J Gastroenterol 2014; 20(43): 16146-16152
URL http://www.wjgnet.com/1007-9327/full/v20/i43/16146.htm
DOI http://dx.doi.org/10.3748/wjg.v20.i43.16146
Full Article (PDF) WJG-20-16146.pdf
Full Article (Word) WJG-20-16146.doc
Manuscript File 9804-Review.doc
Answering Reviewers 9804-Answering Reviewers.pdf
Copyright License Agreement 9804-Copyright Assignment.pdf
Non-Native Speakers of English Editing Certificate Editing_Certificate_20140228114204.pdf
Peer-review Report 9804-Peer reviews.pdf
Scientific Misconduct Check 9804-CrossCheck.jpg
Scientific Editor Work List 9804-Scientific editor work list.pdf