The resulting VICs activation, driven by the NF-κB pathway, leads to the remodelling and dysfunction of the aortic valve, marked by increased matrix metalloproteinaseproduction, extracellular matrix protein synthesis, and up-regulated expression of cell adhesion molecules, integrins, and pro-inflammatory cytokines [45, 46], contributing to the faster disease progression in individuals with DM. Here, NFKB1 is linked to diabetes mellitus.