Review ArticleRole of NFATc1 in the Bone-Vascular Axis Calcification ParadoxGu, Wen MD*; Wang, Zhongqun PhD†; Sun, Zhen MD†; Bao, Zhengyang MD†; Zhang, Lili MD†; Geng, Yue MD†; Jing, Lele MD†; Mao, Xiang MD†; Li, Lihua MD*Author Information Departments of *Pathology; and †Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, China. Reprints: Lihua Li, MD, Department of Pathology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China (email: email@example.com). Supported by the National Natural Science Foundation of China (81770450, 81370408); the related Foundation of Jiangsu Province (WSN-044, LGY2018092, QNRC2016836); the Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions; Postgraduate Research & Practice Innovation Program of Jiangsu Province (SJCX18_0754, SJKY19_2585); Zhenjiang Cardiovascular Clinical Research Center Project (SS2018008); Grant of Jiangsu University (18AD0141). The authors report no conflicts of interest. All authors contributed to conception and design and wrote the review. All authors read and approved the final manuscript. Received August 16, 2019 Accepted December 07, 2019 Journal of Cardiovascular Pharmacology: March 2020 - Volume 75 - Issue 3 - p 200-207 doi: 10.1097/FJC.0000000000000788 Buy Metrics 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. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.