bone marker, osteoprotegerin, rankl, fetuin-a, calcium score, non-coding rnas, Diseases of the circulatory (Cardiovascular) system, RC666-701

Increasing evidence suggests a common physiological process for bone and coronary artery calcification (CAC), implying the role of bone metabolism markers in subclinical atherosclerosis development. However, the association between bone turnover markers and the development of CAC has remained controversial, as seen in various studies. Because CAC measurement has both financial burden and radiation exposure risk in individuals with suspected cardiovascular disease (CVD), applying the diagnostic role of osteogenic markers in predicting abnormal CAC would improve treatment adherence and reduce the rate of CVD mortality. In this review, we begin by describing the current understanding of the molecular mechanisms of bone markers in the etiology of CAC. Furthermore, we summarize bone-associated regulatory factors at the molecular level as novel therapeutic targets for CAC. In addition, we focused on the current results on the prognostic role of novel mediators of osteogenic activity in determining the risk of CAC as a preclinical factor of atherosclerotic CVD. Accumulating evidence suggests the role of bone marker-mediated pathways in the progression of CAC, which may lead to early diagnosis of CVD complications and the establishment of innovative targets for pharmacological therapy. Indeed, miRNAs and lncRNAs, as novel therapeutic interventions, can be a research priority in regulating bone metabolism at the gene expression level to attenuate high CAC and improve CVD outcomes.