Keeping mitochondria happy – benefits of a pore choice in acute pancreatitis
Author:
Affiliation:
1. Department of Cellular & Molecular Physiology, Institute of Translational Medicine University of Liverpool UK
Publisher
Wiley
Subject
Physiology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1113/JP279116
Reference5 articles.
1. Fatty Acid Ethyl Esters Cause Pancreatic Calcium Toxicity via Inositol Trisphosphate Receptors and Loss of ATP Synthesis
2. The Exocrine Pancreas: The Acinar-Ductal Tango in Physiology and Pathophysiology
3. Fatty acid ethyl ester synthase inhibition ameliorates ethanol-induced Ca2+-dependent mitochondrial dysfunction and acute pancreatitis
4. Mechanism of mitochondrial permeability transition pore induction and damage in the pancreas: inhibition prevents acute pancreatitis by protecting production of ATP
5. Novel mitochondrial transition pore inhibitor N ‐methyl‐4‐isoleucine cyclosporin is a new therapeutic option in acute pancreatitis
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2. Precise Control of Metal Active Sites of Metal–Organic Framework Nanozymes for Achieving Excellent Enzyme‐Like Activity and Efficient Pancreatitis Therapy;Small;2024-03-15
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