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Vascular calcification is characterized as the deposition of hydroxyapatite mineral in the form of calcium-phosphate complexes in the vasculature. Transdifferentiation between vascular smooth muscle cells (VSMCs) and osteoblast-like cells is considered essential in the progression of vascular calcification. The pathophysiological mechanisms underlying vascular calcification and VSMC osteogenic differentiation remain to be fully elucidated, and the development of novel therapies is required. In the present study, PCR and western blot analysis were conducted to quantify the mRNA and protein expression levels of calcification-associated markers (bone morphogenetic protein 2, alkaline phosphatase, osteoprotegerin, osteocalcin, and runt-related transcription factor 2) and adropin in VSMCs and rat vascular tissues. The calcification of VSMCs was assessed using alizarin red staining. Moreover, adropin expression levels in VSMCs were analyzed using immunofluorescence. Lentiviral transfection and small interfering RNA were used for overexpression and knockdown of adropin in VSMCs, respectively. The results demonstrated that adropin alleviated vascular calcification in vivo. Moreover, adropin also inhibited osteogenic differentiation and the calcification of VSMCs in vitro. Notably, results of the present study revealed that the tyrosine protein kinase JAK2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway played a key role in the aforementioned inhibition. In conclusion, the results of the present study demonstrated that adropin inhibited VSMC osteogenic differentiation to alleviate vascular calcification via the JAK2/STAT3 signaling pathway.

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Cystatin C is associated with atherosclerosis, but the relationship between cystatin C and coronary artery calcification (CAC) is uncertain. The purpose of this study was to evaluate the predictive value of cystatin C on the occurrence and severity of CAC.A total of 1447 hospitalized patients with coronary computed tomography angiography were selected in this study. According to the CAC score (CACS), patients were divided into calcification group (with CAC, n = 749) and control group (without CAC, n = 698). The calcification group was further divided into low calcification group (CACS < 100, n = 407), medium calcification group (CACS 100-400, n = 203), and high calcification group (CACS≥400, n = 139).Patients with CAC had higher cystatin C level than those in control group (P < .05). With the increase of calcification score, the cystatin C level showed an upward trend. The cystatin C level in the high calcification group was significantly higher than those in the low and medium calcification group (P < .05). ROC curve analysis showed that cystatin C had a high predictive value for the occurrence of CAC [area under the curve 0.640, 95% confidence interval (95% CI) 0.591-0.690, cut-off value 0.945 mg/L, sensitivity 0.683, specificity 0.558, P < .05] and severe CAC (area under the curve 0.638, 95% CI 0.550-0.762, cut-off value 0.965 mg/L, sensitivity 0.865, specificity 0.398, P < .05). Multivariate logistic regression analysis showed that cystatin C was an independent predictor of severe CAC (AOR 3.748, 95% CI 1.138-10.044, P < .05).Cystatin C was significantly associated with the occurrence and severity of CAC, suggesting that cystatin C had the potential as a predictor of CAC. Abbreviations: AOR = adjusted odd ratio, CAC = coronary artery calcification, CACS = coronary artery calcification score, CI = confidence interval, CysC = Cystatin C, eGFR = estimated glomerular filtration rate, IL-6 = interleukin-6, LAD = left anterior descending, LCX = circumflex, LM = left main, MDRD = modification of diet in renal disease trial, OPG = osteoprotegerin, p38MAPK = p38 mitogen-activated protein kinase, RANK = receptor activator of nuclear factor-kB, RANKL = RANK ligand, RCA = right coronary artery, ROC = receiver operating characteristic, TNF-a = tumor necrosis factor-a.

Background Red blood cell (RBC) indices such as RBC count and RBC distribution width (RDW) are associated with heart failure and coronary artery disease, but the relationship between RBC indices and coronary artery calcification (CAC) is unclear. This study aimed to investigate RBC indices’ correlation with, and predictive value for, the presence and severity of CAC. Methods In this study, 1257 hospitalized patients who received a coronary computed tomography angiography examination were finally selected. Patients were classified into a control group (without CAC, n = 655) and a calcification group (with CAC, n = 602) according to their CAC score. The calcification group was further divided into a low calcification group, medium calcification group, and high calcification group. Results In the calcification group, the RBC count was lower, and the RDW-standard deviation (SD) and RDW-coefficient of variation (CV) were higher, than those in the control group (P &lt; .05). In the high calcification group, the RBC count was significantly lower, and the RDW-SD and RDW-CV were significantly higher, than those in the low calcification group (P &lt; .05). Multivariate logistic regression analysis showed that RBC count, RDW-SD, and RDW-CV were independent predictors of CAC presence. Furthermore, multivariate logistic regression analysis also showed that RBC count and RDW-SD were independent predictors of severe CAC. Conclusions RBC indices were significantly associated with the presence and severity of CAC, indicating that these RBC indices have the potential to be predictors of CAC.