Abstract
Nuclear factor of activated T cell cytoplasmic 1 (NFATc1), a crucial member of the transcription factor NFAT family, is indispensable in the immune system and the morphogenesis of cardiac valves and septa and is also vital in osteoclasts and atherosclerotic calcification. Currently, osteoporosis and vascular diseases are severely hazardous to health and quality of life, and the 2 conditions always coincide with each other. The bone-vascular axis calcification paradox serves as a bridge between bone and vascular diseases, linking these 2 seemingly separate diseases, and the receptor activator of NF-κB (RANK)/receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG) system may be the common mechanism of the bone-vascular axis calcification paradox. NFATc1 provides a new therapeutic target for bone and vascular diseases. However, the specific mechanism by which NFATc1 acts on the bone-vascular axis calcification paradox, whether NFATc1 is related to the RANK/RANKL/OPG system, and how to use NFATc1 as a therapeutic target to avoid its side effects in other systems requires further study.
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