ArticleDigestive diseases and sciences2026
Zinc Transporter ZIP7 Is Associated with Intestinal Barrier Injury in Severe Acute Pancreatitis: Potential Roles in Mitochondrial Homeostasis and Ferroptosis.
Article in Digestive diseases and sciences, 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
backgroundSevere acute pancreatitis (SAP) is often accompanied by intestinal mucosal barrier injury (IBI), in which ferroptosis of intestinal epithelial cells plays a critical role. The cellular zinc transporter ZIP7 has been reported to be closely associated with ferroptosis.
aimsThis study aimed to investigate the regulatory role of zinc transporter ZIP7 on ferroptosis and its underlying mechanism in SAP-induced IBI.
methodsSodium taurocholate (5%) was retrogradely perfused into the biliopancreatic duct to establish a model of SAP in rats. Serum-related indicators, lipid peroxidation, and ferroptosis-related markers in intestinal tissues were assessed. Mitochondrial zinc metabolism, membrane potential, and ATP production in intestinal epithelial cells were examined. Histopathological changes were evaluated using hematoxylin and eosin staining, whereas the expressions of ferroptosis-, tight junction-, and mitophagy-related proteins were analyzed by Western blotting and immunofluorescence.
resultsZIP7 expression was upregulated in the intestines of SAP rats. Mechanistically, elevated ZIP7 was accompanied by mitochondrial hyperpolarization and altered PINK1‑Parkin‑related mitophagy, which correlated with impaired ATP production and excessive reactive oxygen species accumulation. These changes were associated with disturbances in iron metabolism and lipid peroxidation, and may contribute to ferroptosis and aggravated intestinal barrier injury. Pharmacological inhibition of ZIP7 using NVS-ZP7-4 restored mitochondrial function, enhanced PINK1-Parkin-mediated mitophagy, and attenuated ferroptosis in intestinal epithelial cells. Furthermore, ZIP7 inhibition reduced serum injury marker levels, alleviated histopathological damage, and improved tight junction protein expression, thereby preserving intestinal barrier function.
conclusionZIP7 inhibition ameliorates SAP‑induced IBI and modulates zinc metabolism, mitochondrial homeostasis, and ferroptosis in rats, suggesting that ZIP7 may represent a potential therapeutic target for SAP‑induced IBI.
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