Diverse Misfolding Mutant Digestive Enzymes Cause Chronic Pancreatitis Through Common Pathways
Our study demonstrates that Cpa1 N256K and Pnlip T221M mice develop CP through similar mechanisms with slight differences in progression and severity. Both models could serve as invaluable tools for developing and testing CP therapies. Targeting cell death pathways for therapy may be unfeasible given their redundancy. Instead, effective therapeutic strategies should focus on reducing the burden of misfolded digestive enzymes in the pancreas.
Authors
- Neel Matiwala
- Jianguo Lin (ORCID: https://orcid.org/0000-0001-9314-596X)
- Xunjun Xiao (ORCID: https://orcid.org/0000-0001-5930-4664)
- Mark E. Lowe (ORCID: https://orcid.org/0000-0002-5116-3841)
- Steven J Wilhelm (ORCID: https://orcid.org/0000-0002-0521-7730)
- Miklós Sahin‐Tóth (ORCID: https://orcid.org/0000-0003-4513-9922)
- Grace Curry (ORCID: https://orcid.org/0000-0001-7132-2099)
- Tam Quach
Institutions
- University of California, Los Angeles (US)
- Washington University in St. Louis (US)
Publication Details
- Journal
- Cellular and Molecular Gastroenterology and Hepatology
- Published
- 2025-09-23
- DOI
- https://doi.org/10.1016/j.jcmgh.2025.101638
- Citations
- 1
- Primary Topic
- Pancreatitis Pathology and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 2.01