JUND is a proto-oncogene encoding an AP-1 transcription factor that heterodimerizes with FOS family proteins to bind AP-1 consensus sequences and regulate gene transcription 12. Beyond its canonical transcriptional role, JUND functions as a critical regulator in multiple disease contexts. In metabolic and inflammatory diseases, JUND expression is significantly dysregulated. In osteoarthritis, JUND is downregulated in synovial tissue and serves as a diagnostic biomarker; its reduced expression correlates with immune infiltration and inflammatory progression 34. Similarly, JUND is suppressed in diabetic cardiomyopathy, where its downregulation is epigenetically controlled through DNA methylation, histone modifications, and miRNA-673-mediated translational repression, leading to increased oxidative stress and cardiac dysfunction 5. Conversely, obesity paradoxically activates JunD, which then drives myocardial lipid accumulation through PPARγ-dependent transcription of lipogenic genes, and this activation is normally restrained by miR-494-3p 6. In immune and cancer contexts, JUND maintains distinct roles. In CD8+ T cells, JunD sustains proliferative capacity and is preserved during combined decitabine and anti-PD-1 therapy, enhancing anti-tumor responses 7. In diabetic retinopathy, JUND is upregulated in circulating immune cells and mediates their pathogenic effects on retinal endothelial cells 8. In glioblastoma, JUND cooperates with IFI16 to activate HMOX1 expression, promoting ferroptosis evasion and radioresistance 9. In bladder cancer, JUND mRNA stability is reduced by high-glucose-associated lactylation of YTHDC1, decreasing NECTIN4 expression and drug sensitivity 10.