ArticleBMC gastroenterology2025
Investigation of the mechanism by which miR-223-3p inhibits reflux esophagitis through targeting the NLRP3 inflammasome.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- The role of microRNAs in gastritis, intestinal metaplasia, and gastric cancer: a narrative review.Translational cancer research · 2025Review
- Molecular insights into NLRP3 inflammasome and miRNA modulation in oral cancer.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundReflux esophagitis is a common gastrointestinal disorder characterized by significant inflammatory responses. The NLRP3 inflammasome plays a crucial role in inflammation, and miR- 223 - 3p has been found to inhibit its expression by targeting NLRP3 mRNA. This study aims to further investigate the mechanism by which miR- 223 - 3p inhibits reflux esophagitis through targeting the NLRP3 inflammasome.
methodsA reflux esophagitis cell model was constructed to assess the expression levels of miR- 223 - 3p and NLRP3. Overexpression and inhibition techniques were used to study the effects of miR- 223 - 3p on the NLRP3 inflammasome. qPCR and Western blot analyses were employed to detect the expression of related inflammatory factors, and flow cytometry was used to assess cell apoptosis and cell cycle changes.
resultsThe study found that miR- 223 - 3p was significantly downregulated in the reflux esophagitis model, while NLRP3 and its downstream inflammatory factors were significantly upregulated. Overexpression of miR- 223 - 3p markedly inhibited NLRP3 expression, reduced the release of inflammatory factors, decreased cell apoptosis, promoted cell cycle progression, and enhanced cell viability. Overexpression of NLRP3 reversed these protective effects of miR- 223 - 3p, further confirming that miR- 223 - 3p alleviates inflammation by inhibiting the activation of the NLRP3 inflammasome.
conclusionThis study demonstrates that miR- 223 - 3p plays a key role in reducing inflammation and cellular damage in reflux esophagitis by targeting the NLRP3 inflammasome. These findings provide new insights and potential therapeutic targets for the treatment of reflux esophagitis.
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