In line with this paradigm, our synthesis highlights that the dysregulation of adipokines and vascular modulators (RBP4, LCN2, ApoM, Klotho and MGP) converges on shared molecular hubs—oxidative stress, endothelial dysfunction, lipid dysregulation and vascular calcification—reflecting the cross-organ mechanisms described by the AHA. The gene discussed is LCN2; the disease is endothelial dysfunction.