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Autophagy and pancreatitis
Anna S Gukovskaya1, Ilya Gukovsky
1Veterans Affairs Greater Los Angeles Healthcare System and University of California at Los Angeles, Los Angeles, CA 90073, USA. agukovsk@ucla.edu
American Journal of Physiology. Gastrointestinal and Liver Physiology
|September 11, 2012
Summary
Impaired cellular degradation, known as autophagy, and defective lysosomes are key factors in acute pancreatitis. Understanding these mechanisms may reveal new therapeutic targets for this serious pancreatic disease.
Area of Science:
- Cell Biology
- Gastroenterology
- Pathophysiology
Background:
- Acute pancreatitis is a severe pancreatic inflammatory disease with high morbidity and mortality.
- The underlying pathophysiology of acute pancreatitis is not fully understood.
- Autophagy, a crucial cellular degradation process, plays a role in pancreatic health.
Purpose of the Study:
- To review recent findings on the role of autophagy and lysosomal function in acute pancreatitis.
- To propose lysosomal/autophagic dysfunction as a central event in pancreatitis.
- To identify potential therapeutic targets for pancreatitis.
Main Methods:
- Review of experimental models and genetically altered mice studies.
- Analysis of cellular degradative pathways, specifically autophagy and lysosomal function.
- Synthesis of current evidence linking autophagy to pancreatitis.
Main Results:
- Autophagy is impaired in acute pancreatitis.
- Defective lysosomal function is a significant cause of impaired autophagy in pancreatitis.
- Lysosomal/autophagic dysfunction is proposed as a key initiating event and converging point in pancreatitis.
Conclusions:
- Lysosomal/autophagic dysfunction is a critical factor in the pathophysiology of acute pancreatitis.
- Further research into upstream and downstream mechanisms is needed.
- Targeting lysosomal and autophagic pathways may offer novel therapeutic strategies for pancreatitis.