ArticleAutophagy2025
Deletion of the WD40 domain of ATG16L1 exacerbates acute pancreatitis, abolishes LAP-like non-canonical autophagy and slows trypsin degradation.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- LC3B Mediated SETDB1-Accounted Alcoholic Steatohepatitis via Lipidation-Dependent LAP and Lipidation-Independent Nuclear Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Autophagy dysfunction in pancreatic acinar cells in acute pancreatitis: from molecular mechinery and trypsinogen activation to heterogeneity and therapeutic implications.Journal of molecular histology · 2026Review
- Breaking the Calcium Overload Cycle in Acute Pancreatitis: Emerging Pharmacological Strategies.Digestive diseases and sciences · 2026Review
- stGrads: decoding spatial gene expression gradients through proximity-driven analysis in complex tissues.Briefings in bioinformatics · 2026Article
- From gut to pancreas: Shared genetic susceptibility and biological convergence in acute pancreatitis and Crohn's disease.PloS one · 2026Article
- From micro to macro, nanotechnology demystifies acute pancreatitis: a new generation of treatment options emerges.Journal of nanobiotechnology · 2025Review
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Authors and funding
8 authors.
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Abstract
The WD40 domain (WDD) of ATG16L1 plays a pivotal role in non-canonical autophagy. This study examined the role of recently identified LAP-like non-canonical autophagy (LNCA) in acute pancreatitis. LNCA involves rapid single-membrane LC3 conjugation to endocytic vacuoles in pancreatic acinar cells. The rationale for this study was the previously observed presence of trypsin in the organelles undergoing LNCA; aberrant trypsin formation is an important factor in pancreatitis development. Here we report that the deletion of WDD (attained in ATG16L1[E230] mice) eliminated LNCA, aggravated caerulein-induced acute pancreatitis and suppressed the fast trypsin degradation observed in both a rapid caerulein-induced disease model and in caerulein-treated isolated pancreatic acinar cells. These experiments indicate that LNCA is a WDD-dependent mechanism and suggest that it plays not an activating but a protective role in acute pancreatitis. Furthermore, palmitoleic acid, another inducer of experimental acute pancreatitis, strongly inhibited LNCA, suggesting a novel mechanism of pancreatic lipotoxicity.
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