Bony Heart: Myocardial and pericardial calcification, the yet unrevealed mechanism

The pulsatile organ, heart consists of cells possessing different functions during developmental stages and in adult, lack of which causes pathological condition. Previous studies show increased alkaline phosphatase (ALP), osteopontin expression in atherosclerosis and vascular calcification, increased reactive oxygen species (ROS) generation and Runt-related transcription factor-2 (Runx2), osteocalcin during aortic valve calcification, increased Runx2, osteopontin in cardiac fibroblasts upon osteogenic induction. Recent findings indicate that cardiomyocytes too take osteoblastic phenotype during hypertrophy. Cardiac injuries including hypertrophy, oxidative stress make the cells prone to calcification. This review mainly focusses on the current knowledge of the osteoblastic modification of cardiac cells with special emphasis on the rare cases of myocardial, pericardial and fetal cardiac calcification. Since cardiomyocyte and pericardial calcification are rare but gradually increasing phenomenon, better understanding of the associated molecular mechanism is needed for therapeutic intervention and in targeting specific molecules for treating or slowing down the calcification process.