New Insights into Acute Pancreatitis
A special issue of Gastroenterology Insights (ISSN 2036-7422). This special issue belongs to the section "Pancreas".
Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 551
Special Issue Editors
Interests: cell biology; immunology; molecular biology; single cell regulatory networks
Special Issue Information
Dear Colleagues,
Acute pancreatitis is life threatening inflammation of the pancreas affecting 1 in 3000 people that impairs the long-term quality of life with repeated hospitalizations. The most frequent cause of acute pancreatitis is gallstone complications releasing bile acids in the pancreas leading to cell death due to dysregulated calcium signaling. Further alcohol intake also disrupts calcium signaling, leading to dysregulation of mitochondrial function and cell death. Acute pancreatitis is characterized by impaired autophagy, causing cell apoptosis and necrosis. The necrotic cells release cytokines that mediate monocyte activation, leading to inflammasome formation. Triglycerides hydrolyzed by lipase into unsaturated fatty acids contribute to acute pancreatitis. There is increased endoplasmic reticulum stress in acute pancreatitis due to unfolded protein accumulation. Diabetes and exocrine pancreatic insufficiency are common complications after acute pancreatitis. Characterization of dysregulated cellular pathways and identifying the pathophysiological mechanisms underlying acute pancreatitis will guide the identification of potential targets for future therapeutic trials.
This Special Issue aims to identify the pathophysiological mechanisms and the cellular signaling pathways in acute pancreatitis. Papers addressing these topics are invited for this Special Issue, especially those deciphering pathophysiological mechanisms that can be potential therapeutic targets.
Dr. Ankita Srivastava
Dr. Santosh Kumar Yadav
Guest Editors
Manuscript Submission Information
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Keywords
- acute pancreatitis
- gallstones
- alcohol intake
- bile acids
- calcium signalling
- apoptosis
- inflammasome
- autophagy
- triglycerides
- mitochondrial function
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