KLF2, regulated by H-ferritin and iron, inhibits aortic valve calcification and inflammation via controlling activity of RUNX2 and nuclear factor-kappa B in valvular interstitial cells

Remodeling of valvular tissues in calcific aortic valve disease involves the activation of two principal transcription factors: runt-related transcription factor 2 (RUNX2), responsible for osteoblast differentiation, and nuclear factor-kappa B, responsible for inflammatory responses. We hypothesized that the expression of H-ferritin in valvular interstitial cells regulates the activity of RUNX2 and nuclear factor-kappa B via Kruppel-like factor 2 , thereby connecting cellular iron metabolism to calcification.