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Published Online: 11 October 2011

Calcium and Reactive Oxygen Species in Acute Pancreatitis: Friend or Foe?

Publication: Antioxidants & Redox Signaling
Volume 15, Issue Number 10

Abstract

Significance: Acute pancreatitis (AP) is a debilitating and, at times, lethal inflammatory disease, the causes and progression of which are incompletely understood. Disruption of Ca2+ homeostasis in response to precipitants of AP leads to loss of mitochondrial integrity and cellular necrosis. Recent Advances: While oxidative stress has been implicated as a major player in the pathogenesis of this disease, its precise roles remain to be defined. Recent developments are challenging the perception of reactive oxygen species (ROS) as nonspecific cytotoxic agents, suggesting that ROS promote apoptosis that may play a vital protective role in cellular stress since necrosis is avoided. Critical Issues: Fresh clinical findings have indicated that antioxidant treatment does not ameliorate AP and may actually worsen the outcome. This review explores the complex links between cellular Ca2+ signaling and the intracellular redox environment, with particular relevance to AP. Future Directions: Recent publications have underlined the importance of both Ca2+ and ROS within the pathogenesis of AP, particularly in the determination of cell fate. Future research should elucidate the subtle interplay between Ca2+ and redox mechanisms that operate to modulate mitochondrial function, with a view to devising strategies for the preservation of organellar function. Antioxid. Redox Signal. 15, 2683–2698.

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cover image Antioxidants & Redox Signaling
Antioxidants & Redox Signaling
Volume 15Issue Number 10November 15, 2011
Pages: 2683 - 2698
PubMed: 21861696

History

Published in print: November 15, 2011
Published online: 11 October 2011
Published ahead of print: 23 August 2011
Accepted: 5 July 2011
Revision received: 13 June 2011
Received: 10 March 2011

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David M. Booth
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, United Kingdom.
Liverpool NIHR Pancreas Biomedical Research Unit, Royal Liverpool University Hospital, University of Liverpool, Liverpool, United Kingdom.
Rajarshi Mukherjee
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, United Kingdom.
Liverpool NIHR Pancreas Biomedical Research Unit, Royal Liverpool University Hospital, University of Liverpool, Liverpool, United Kingdom.
Robert Sutton
Liverpool NIHR Pancreas Biomedical Research Unit, Royal Liverpool University Hospital, University of Liverpool, Liverpool, United Kingdom.
David N. Criddle
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, United Kingdom.

Notes

Address correspondence to:Dr. David N. CriddleDepartment of Cellular and Molecular PhysiologyInstitute of Translational MedicineFaculty of Health and Life SciencesUniversity of LiverpoolCrown St.Liverpool L69 3BXUnited Kingdom
E-mail: [email protected]

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