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World J Gastroenterol. Nov 14, 2013; 19(42): 7231-7240
Published online Nov 14, 2013. doi: 10.3748/wjg.v19.i42.7231
Published online Nov 14, 2013. doi: 10.3748/wjg.v19.i42.7231
Figure 3 A scheme representing the role of digestive enzymes in normal pancreatic tissue and in the case of pancreatitis.
A: In a normal pancreas, SPINK1 (first line of defense) and mesotrypsin (second line of defense) inhibit the generation of trypsin resulting from auto-activation of trypsinogen. These defense mechanisms prevent the pancreas from activating the pancreatic enzyme cascade and auto-digestion; B: If mutations are present in the SPINK1 and/or in the mesotrypsin gene, they losses their ability to inhibit the generation of trypsin resulting in activation of enzyme cascade and subsequent pancreatic auto-digestion leading to pancreatitis. SPINK1: Serine protease inhibitor, kazal type 1, gene (encodes for pancreatic secretory trypsin inhibitor).
- Citation: Brock C, Nielsen LM, Lelic D, Drewes AM. Pathophysiology of chronic pancreatitis. World J Gastroenterol 2013; 19(42): 7231-7240
- URL: https://www.wjgnet.com/1007-9327/full/v19/i42/7231.htm
- DOI: https://dx.doi.org/10.3748/wjg.v19.i42.7231