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David N. Criddle
Researcher at University of Liverpool
Publications - 116
Citations - 4361
David N. Criddle is an academic researcher from University of Liverpool. The author has contributed to research in topics: Acinar cell & Acute pancreatitis. The author has an hindex of 37, co-authored 111 publications receiving 3869 citations. Previous affiliations of David N. Criddle include State University of Ceará & University of Manchester.
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Journal ArticleDOI
Fatty Acid Ethyl Esters Cause Pancreatic Calcium Toxicity via Inositol Trisphosphate Receptors and Loss of ATP Synthesis
David N. Criddle,J. A. Murphy,Gregorio Fistetto,Stephanie L. Barrow,Alexei V. Tepikin,John P. Neoptolemos,Robert Sutton,Ole H. Petersen +7 more
TL;DR: Fatty acid ethyl ester increases through inositol trisphosphate receptors and, following hydrolysis, through calcium-ATPase pump failure from impaired mitochondrial ATP production, and lowering cellular fatty acid substrate concentrations may reduce cell injury in pancreatitis.
Journal ArticleDOI
Ethanol toxicity in pancreatic acinar cells: Mediation by nonoxidative fatty acid metabolites
David N. Criddle,Michael Raraty,John P. Neoptolemos,Alexei V. Tepikin,Ole H. Petersen,Robert Sutton +5 more
TL;DR: It is concluded that nonoxidative fatty acid metabolites, rather than ethanol itself, are responsible for the marked elevations of [Ca(2+)](i) that mediate toxicity in the pancreatic acinar cell and that these compounds act primarily by releasing Ca(2+) from the endoplasmic reticulum.
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Calcium signalling and pancreatic cell death: apoptosis or necrosis?
David N. Criddle,Julia Vladimirovna Gerasimenko,Heidi K. Baumgartner,M. Jaffar,Svetlana Voronina,Robert Sutton,Ole H. Petersen,Oleg Vsevolodovich Gerasimenko +7 more
TL;DR: Apoptosis, induced by menadione or bile acids, is potentiated by inhibition of an endogenous detoxifying enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1), suggesting its importance as a defence mechanism that may influence cell fate.
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Mechanism of mitochondrial permeability transition pore induction and damage in the pancreas: inhibition prevents acute pancreatitis by protecting production of ATP
Rajarshi Mukherjee,Rajarshi Mukherjee,Olga A. Mareninova,Irina V. Odinokova,Irina V. Odinokova,Wei Huang,Wei Huang,Wei Huang,J. A. Murphy,J. A. Murphy,Michael Chvanov,Michael Chvanov,Muhammad A. Javed,Muhammad A. Javed,Li Wen,Li Wen,David Booth,David Booth,Matthew C Cane,Muhammad Awais,Muhammad Awais,Bruno Gavillet,Rebecca M. Pruss,Sophie Schaller,Jeffery D. Molkentin,Alexei V. Tepikin,Alexei V. Tepikin,Ole H. Petersen,Stephen J. Pandol,Ilya Gukovsky,David N. Criddle,David N. Criddle,Anna S. Gukovskaya,Robert Sutton,Robert Sutton +34 more
TL;DR: The mechanism and consequences of MPTP opening are demonstrated to be fundamental to multiple forms of acute pancreatitis and validates the MPTP as a drug target for this disease.
Journal ArticleDOI
Inhibitors of ORAI1 Prevent Cytosolic Calcium-Associated Injury of Human Pancreatic Acinar Cells and Acute Pancreatitis in 3 Mouse Models.
Li Wen,Svetlana Voronina,Muhammad A. Javed,Muhammad Awais,Peter Szatmary,Peter Szatmary,Diane Latawiec,Michael Chvanov,D. Collier,Wei Huang,John Barrett,Malcolm Begg,Kenneth A. Stauderman,Jack Roos,Sergey Grigoryev,Stephanie Ramos,Evan Rogers,Jeff Whitten,Gonul Velicelebi,Michael Dunn,Alexei V. Tepikin,David N. Criddle,Robert Sutton +22 more
TL;DR: Cytosolic calcium overload, mediated via ORAI1, contributes to the pathogenesis of acute pancreatitis.