Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon?

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Nov 7, 2024 (publication date) through Feb 7, 2025

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Nov 7, 2024; 30(41): 4417-4438
Published online Nov 7, 2024. doi: 10.3748/wjg.v30.i41.4417

Table 3 Genetic autophagy blockade increases the basal trypsin activity in the pancreas

Knockout mouse	Function of ablated protein	Effect of the knockout on autophagy	Fold increase in trypsin activity	Ref.
Atg7^Δpan	Key mediators of autophagosome formation	Blockade of autophagosome formation and autophagy	2.5	[186]
Atg5^Δpan			2.0	[187]
VMP1^Δac			3.5	[188]
LAMP2 KO	Major lysosomal membrane protein	Lysosomal dysfunction. Autophagy blockade	3.0	[135]
GNPTAB KO	Mediator of hydrolase delivery to lysosomes	Lysosomal and endosomal dysfunction. Autophagy blockade	8.0	[143]
Tfeb^Δac; Tfe3^-/-	Transcriptional regulator of lysosomal biogenesis, autophagy	Autophagy blockade	2.5	[140,146]

Citation: Gukovskaya AS, Lerch MM, Mayerle J, Sendler M, Ji B, Saluja AK, Gorelick FS, Gukovsky I. Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon? World J Gastroenterol 2024; 30(41): 4417-4438
URL: https://www.wjgnet.com/1007-9327/full/v30/i41/4417.htm
DOI: https://dx.doi.org/10.3748/wjg.v30.i41.4417