Fig. 7.

Proposed working model summarizing the molecular mechanism by which miR-21 modulates inflammatory injury in P.g-LPS-stimulated HUVECs. Downregulation of miR-21 upregulates PDCD4, which activates NF-κB/iNOS/NO signaling, resulting in increased apoptosis and inflammation. In contrast, miR-21 overexpression inhibits this axis, restoring endothelial function and reducing proinflammatory responses. Abbreviations: miR-21 = microRNA-21; PDCD4 = Programmed Cell Death Protein 4; NF-κB = Nuclear Factor kappa-light-chain-enhancer of activated B cells; iNOS = inducible Nitric Oxide Synthase; NO = Nitric Oxide; P.g-LPS = Porphyromonas gingivalis lipopolysaccharide; HUVECs = Human Umbilical Vein Endothelial Cells.