Vitamin A enhances PI3K/Akt signaling and mitigates enterocyte apoptosis in a mouse model of necrotizing enterocolitis
Topic overview
This preclinical study demonstrates that vitamin A supplementation reduces intestinal cell death in a mouse model of necrotizing enterocolitis (NEC) by activating the PI3K/Akt survival pathway and modulating apoptotic proteins. The findings suggest vitamin A may offer therapeutic potential for preventing enterocyte damage in this devastating neonatal intestinal disease.
Key takeaways
- NEC pathogenesis involves downregulation of PI3K/Akt survival signaling and upregulation of pro-apoptotic factors (Bax, CytoC, Caspase 3).
- Vitamin A supplementation restores PI3K/Akt pathway activity and reduces enterocyte apoptosis in experimental NEC models.
- Vitamin A shifts the apoptotic balance by increasing anti-apoptotic Bcl-2 while decreasing pro-apoptotic mediators.
- Therapeutic vitamin A may protect intestinal epithelium in NEC through modulation of cell survival signaling pathways.
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How to cite: GlobalCastMD. Vitamin A enhances PI3K/Akt signaling and mitigates enterocyte apoptosis in a mouse model of necrotizing enterocolitis. GlobalCastMD Medical Library. 2025-01-08. https://dev.library.globalcastmd.com/article/9618?via_space=staycurrentmd
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