Publication

Abstract :

Cardiac valve stenosis and calcification is estimated to affect over 500 million people by 2050 (d’Arcy et al., 2016). Calcification refers to the mineralization in soft tissues causing hardening of the same. During calcification, the bone-forming progenitors get activated, differentiate into osteocytes, and deposit calcium and other minerals in the tissue (Pillai et al., 2017). In valve tissue, valve interstitial cells (VICs) and valve endothelial cells (VECs) direct the mineralization process, where quiescent progenitors get activated and subsequently differentiate into osteoblast-like cells with activation of pro-osteogenic molecular signaling pathways (Liu et al., 2007). Calcified valve tissue blocks the outflow tract in the heart, resulting in fluid retention, increased resistance, and maladaptive cardiac hypertrophy, eventually leading to heart failure and fatal consequences (Dweck et al., 2012). Currently, no drugs are available to reverse calcification of valves, resulting in surgical replacement as the only treatment option. Aging, chronic inflammation, genetic causes such as notch insufficiency, chronic kidney diseases, anatomical abnormalities, and other acquired modifications in coding and non-coding genes are associated with calcification.