Dataset for <b>miR-433-3p protects against cadmium-induced intestinal injury via targeting </b><b><i>MAPK8</i></b><b> to repress the JNK-JUN signaling pathway</b>

Mechanistically, Cd activated the JNK/MAPK8-JUN pathway, while miR-433-3p restoration suppressed this cascade. Bioinformatics prediction combined with dual-luciferase reporter assays verified <i>MAPK8</i> as a direct target of miR-433-3p. In Cd-challenged mice, <i>in vivo</i> administration of miR-433-3p mimics significantly repressed JNK/MAPK8-JUN signaling activation, thereby ameliorating Cd-provoked intestinal damage and inflammatory responses.

Collectively, our findings <a href="" target="_blank">reveal a previously unrecognized post-transcriptional regulatory mechanism</a>: Cd-driven miR-433-3p reduction de-represses MAPK8 to hyperactivate the JNK-JUN inflammatory cascade, where miR‑433‑3p serves as a critical negative regulator (molecular brake) of this inflammatory axis. Our study provides new insights into Cd-induced intestinal injury and suggests miR-433-3p as a potential therapeutic target against heavy-metal-associated intestinal toxicity.</p><p><br></p>