ArticleJournal of physiology and biochemistry2026
GSDMD palmitoylation induces acinar cell pyroptosis via promoting GSDMD-N oligomerization to aggravate hyperlipidemic acute pancreatitis.
Article in Journal of physiology and biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pancreatic acinar cell pyroptosis played a key role in acute pancreatitis (AP), while the underlying molecular mechanisms were unclear. In this study, hyperlipidemic acute pancreatitis (HLAP) model mice and primary acinar cells were employed for the in vivo and in vitro experiments, respectively. Western blot was employed to assess Gasdermin D-N-terminal pore-forming domain (GSDMD-N) oligomerization; Flow cytometry was employed to assess cell pyroptosis; Immunofluorescence was performed to assess GSDMD-N location in the cytoplasm; HE and TUNEL staining were employed to assess the pathological changes and cell apoptosis of pancreatic tissues. Palmitic acid levels were elevated in serum and pancreatic tissues of HLAP mice, palmitoyltransferase Zinc Finger DHHC Domain-Containing Protein 13 (ZDHHC13) and ZDHHC15 expression levels were markedly increased in primary acinar cells of HLAP mice. Acinar cells of HLAP mice exhibited the increased pyroptosis, which was evidenced by the increased cleaved-caspase-1 and GSDMD-N protein levels, Interleukin (IL)-1β, IL-18, and lactate dehydrogenase (LDH) release, GSDMD-N oligomerization, and caspase-1
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