Valvular heart disease is a leading cause of morbidity and mortality and mechanisms of preservation and restoration of valvular homeostasis are
incompletely understood. Valvular homeostasis is governed by a distinct cell population - valvular interstitial cells (VICs). VICs actively modify
the valves' extracellular matrix (ECM) to maintain integrity of the valvular function under dynamic physiological conditions. Exposed to pathological
stressors, VICs undergo differentiation to form contractile and ECM modifying myofibroblastic and calcification-producing osteoblast-like phenotypes
resulting in progressive fibrosis and accumulation of mineral in the heart valves, ultimately necessitating valve replacement due to severe narrowing
of the orifice (i.e. stenosis).
Identification and characterization of the valvular cell populations can reveal new alleys towards the diagnosis and treatment of valvular heart
disease and inform the design of optimal replacement crafts.
