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Reynolds, J. L. et al. Multifunctional roles for serum protein fetuin-a in inhibition of human vascular smooth muscle cell calcification.
Liu H, Li X, Qin F, Huang K. Selenium suppresses oxidative-stress-enhanced vascular smooth muscle cell calcification by inhibiting the activation of the PI3K/AKT and ERK signaling pathways and endoplasmic reticulum stress.
Vascular smooth muscle cell calcification is associated with major adverse cardiovascular events while indoxyl sulfate has been found to promote vascular smooth muscle cell calcification (Zhang et al., 2018).
Furthermore, adiponectin inhibits macrophage activation [37], [38] and foam cell formation [39], promotes the clearance of early apoptotic cells by macrophages [40], inhibits smooth muscle cell proliferation [32], [41] and antagonizes the stimulatory effect of TNF-α on vascular smooth muscle cell calcification [42].
50 Li et al 51 demonstrated direct protection from vascular calcifications with paricalcitol, and found that paricalcitol could influence proteins involved in the smooth muscle cell calcification process, including bone morphogenetic protein-2 (BMP2), tumor necrosis factor-alpha, and osteopontin.
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Furthermore, an exosome-mediated link between systemic calcium deregulation, smooth muscle cells calcification and increased vessel stiffness has also been made by analysing data in chronic kidney disease patients [ 60].
Recent study has demonstrated that the activation of glucagon-like peptide-1 receptor can inhibit vascular smooth muscle cells calcification through NF-κB/RANKL signaling [ 33] and chronic stimulation of AT4 and inhibition of AT2 receptors reverse diabetes-induced endothelial dysfunction [ 34], which could also play a vital role in renal sodium handling.
Cardús et al 68 tested the effects of calcitriol and paricalcitol on vascular smooth muscle-cell calcification in an animal end-stage renal disease model, and concluded that calcitriol, but not paricalcitol, increased calcification of vascular smooth muscle cells, independently of the levels of calcium and phosphate.
Repression of miR-29a/b upregulated the expression of ADAMTS-7, and subsequently induced vascular smooth muscle cell (VSMC) calcification.
On the other hand, sclerostin has been demonstrated to be upregulated during vascular smooth muscle cell (SMC) calcification in vitro [ 8].
In an in vitro model of the microangiopathy, interferon- α enhanced vascular smooth muscle cell-derived calcifications.
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