Vitamin D in Vascular Calcification: A Double-Edged Sword?

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Term Occurence Count Dictionary
cholecalciferol 2 endocrinologydiseasesdrugs
hypervitaminosis D 3 endocrinologydiseases
rickets 1 endocrinologydiseases
Hypervitaminosis 2 endocrinologydiseases
calcifediol 14 endocrinologydiseasesdrugs
calciphylaxis 1 endocrinologydiseases
calcitriol 13 endocrinologydiseasesdrugs
paricalcitol 2 endocrinologydiseasesdrugs
vascular calcification 4 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
calcifediol 19200 of four cytochrome P450 enzymes (namely vitamin D 25-hydroxylase, or CYP2R1) in the liver to produce calcifediol (25-hydroxyvitamin D), a pre-hormone generally used as the biomarker to indicate vitamin D status. Calcifediol,
calcifediol 20180 [[73],[74]]. Lack of synthesis of precursors in the skin primarily leads to inadequate production of calcifediol , which consequently results in reduced downstream effects. Therefore, correction of deficiency generally
calcifediol 20332 downstream effects. Therefore, correction of deficiency generally involves direct supplementation of calcifediol . While deficiency is widely noted, excess levels of vitamin D, or vitamin D toxicity, has also been
calcifediol 20688 not been associated with excessive sunlight exposure, but more so with abnormal supplementation of calcifediol as over-production of inactive cholecalciferol in the skin does not result in over-production of calcifediol
calcifediol 20797 calcifediol as over-production of inactive cholecalciferol in the skin does not result in over-production of calcifediol [[76],[77]]. Excess supplementation of calcefidiol however, leads to saturation of free calcifediol
calcifediol 20897 calcifediol [[76],[77]]. Excess supplementation of calcefidiol however, leads to saturation of free calcifediol levels that exceeds DBP binding capacity, which then directly induces gene expression and functional
calcifediol 21078 gene expression and functional changes in target cells [[78]]. Therefore, while supplementation of calcifediol is an accepted form of treatment for vitamin deficiency, the process should be tightly monitored to
calcifediol 32240 development using an apolipoprotein E knockout mouse model [[83]]. While mice fed with a diet deficient in calcifediol (25-hydroxyvitamin D) developed increased aortic calcification density, those treated with paricalcitol,
calcifediol 32629 calcium and phosphate levels from paricalcitol-treated mice, but not from those that were given the calcifediol -deficient diet. Furthermore, replenishment of calcifediol levels in calcifediol-deficient mice reduced
calcifediol 32687 mice, but not from those that were given the calcifediol-deficient diet. Furthermore, replenishment of calcifediol levels in calcifediol-deficient mice reduced the extent of calcification, but did not induce any changes
calcifediol 32709 that were given the calcifediol-deficient diet. Furthermore, replenishment of calcifediol levels in calcifediol -deficient mice reduced the extent of calcification, but did not induce any changes in systemic calcium
calcifediol 35526 vitamin D and cardiovascular mortality is well established. Deficient vitamin D levels, in the form of calcifediol , has been linked with increased cardiovascular and non-cardiovascular mortality in a number of large-scale
calcifediol 35785 [[76]]. The predominant finding from these studies is a non-linear, inverse relationship between serum calcifediol concentration in patients and cardiovascular risk, with levels below 24 ng/mL in particular exhibiting
calcifediol 36004 highest relative risk scores [[111],[112],[113],[114],[115],[116]]. In one prospective study, serum calcifediol concentrations of less than 20 ng/mL in pre-hospitalised patients were associated with increased odds
calcitriol 5688 exacerbated in CKD-induced mice by supplementation of a high-phosphate diet and periodic administration of calcitriol (1,25-dihydroxyvitamin D3). Lomashvili et al. were then able to elegantly demonstrate that upon dissecting
calcitriol 19567 cytochrome P450 enzyme, 1α-hydroxylase (CYP27B) in the kidneys to produce the active vitamin D metabolite, calcitriol (1,25-dihydroxyvitamin D3), which ultimately elicits the effects of vitamin D by binding and signalling
calcitriol 21578 activity, given the nature of its metabolism and signalling. For example, production of active vitamin D ( calcitriol ) in the kidneys is tightly regulated through feedback mechanisms on 1α-hydroxylase activity, such as
calcitriol 24463 (unpublished). In addition to precursor forms of vitamin D, such as D2 and D3, dosing of its active metabolite, calcitriol , also produces diffuse and widespread soft tissue calcification that has been demonstrated in a time-dependent
calcitriol 25168 which as previously discussed, lead to vascular osteogenesis and mineralisation. On the other hand, calcitriol has been shown to directly induce mineralisation of bovine VSMCs via the VDR in vitro in a dose-dependent
calcitriol 25823 Increased MMP-9 expression was detected within the chondro-osseous junction of tibias of mice treated with calcitriol in comparison with controls [[91]]. A major limitation which has impeded further clarification of how
calcitriol 26746 ectopic calcification within soft tissue have been detected despite low levels of serum calcium and calcitriol , and instead have been associated with extremely high levels of PTH and inorganic phosphate [[95]].
calcitriol 28488 induction of TNF-α expression [[93]]. The authors furthermore demonstrated that supplementation with calcitriol or the vitamin D analogue maxacalcitol reduced TNF-α levels in accordance with suppressed VSMC mineralisation.
calcitriol 29843 its potential to directly inhibit the osteogenic differentiation process of VSMCs [[94]]. Finally, calcitriol and other vitamin D analogues can reduce the expression of the calcification promoters MMP-2, MMP-9
calcitriol 32372 D) developed increased aortic calcification density, those treated with paricalcitol, an analogue of calcitriol (1,25-dihydroxyvitamin D3), also developed severe calcification. Interestingly, calcification outcomes
calcitriol 43114 expression of TNF-α and osteoblast differentiation factors.[[93],[94]]AnimalLow free levels of calcium and calcitriol in association with high levels of PTH and inorganic phosphate. Stimulation of the expression of TNF-α
calcitriol 43423 of calcium and phosphate levels[[83],[95],[96],[97]]HumanDirect regulation of osteoblast function by calcitriol dependent on serum levels. Increase in the levels of high sensitivity C-reactive protein[[92],[98]]Vitamin
calcitriol 43868 derivatives[[100],[101]]VDR signallingIn vitroSuppression of the expression of osteogenic factors through calcitriol -mediated VDR activation and subsequent signalling[[94]]AnimalStimulation of the expression of osteogenic
cholecalciferol 19000 is through skin synthesis from exposure to ultraviolet radiation. The inactive precursor, known as cholecalciferol (vitamin D3) that is initially produced promptly undergoes 25-hydroxylation by one of four cytochrome
cholecalciferol 20731 sunlight exposure, but more so with abnormal supplementation of calcifediol as over-production of inactive cholecalciferol in the skin does not result in over-production of calcifediol [[76],[77]]. Excess supplementation of
paricalcitol 32343 calcifediol (25-hydroxyvitamin D) developed increased aortic calcification density, those treated with paricalcitol , an analogue of calcitriol (1,25-dihydroxyvitamin D3), also developed severe calcification. Interestingly,
paricalcitol 32563 calcification outcomes were associated with alterations in plasma calcium and phosphate levels from paricalcitol -treated mice, but not from those that were given the calcifediol-deficient diet. Furthermore, replenishment
Select Disease Character Offset Disease Term Instance
Hypervitaminosis 23164 deficient levels of vitamin D potentially leading to deleterious calcification outcomes [[82],[83]].5.1. Hypervitaminosis D and VCInduction of calcification through hypervitaminosis with vitamin D has been demonstrated and
Hypervitaminosis 42660 vascular calcification (VC).Aspect of Vitamin D ExaminedStudy ModelProposed Mechanisms for VCReference No. Hypervitaminosis In vitroModulation of alkaline phosphatase activity, RANKL/OPG ratio and PTH-related peptide expression[[89]]AnimalIncrease
calciphylaxis 3428 calcification) [[11],[12]]. A rare and obliterative form of VC known as calcific uremic arteriolopathy, or calciphylaxis , occurs almost exclusively within end-stage renal disease (ESRD) patients, and is characterised by extensive
hypervitaminosis D 22758 remains controversial to this day. While a large number of studies suggest that vitamin D excess (i.e., hypervitaminosis D ) is associated with extensive calcification, others report that deficiency also promotes calcification,
hypervitaminosis D 37642 deficiency, limited as they may be, studies which have independently examined the relationship between hypervitaminosis D and calcification in patients are also scarce. This may be largely due to the fact that hypervitaminosis
hypervitaminosis D 37749 hypervitaminosis D and calcification in patients are also scarce. This may be largely due to the fact that hypervitaminosis D is rarely seen in human populations, and also that the induction of vitamin D toxicity in patients is
rickets 18530 liver, bone and kidneys. As such, its deficiency is often associated with bone-mineral disorders such as rickets and osteomalacia. Vitamin D has also been reported to serve non-skeletal functions, the majority of
vascular calcification 820 well as poorer patient outcomes. Due to the current limited understanding of the pathophysiology of vascular calcification , the development of effective preventative and therapeutic strategies remains a significant clinical
vascular calcification 1139 such as left ventricular hypertrophy and dyslipidaemia, fail to account for clinical observations of vascular calcification . Therefore, more complex underlying processes involving physiochemical changes to mineral balance, vascular
vascular calcification 42058 1Schematic comparing the original and newly proposed models behind vitamin D’s biphasic response on vascular calcification . (Top panel): Original model concerning that perturbation of systemic vitamin D levels determine calcification
vascular calcification 42554 parathyroid hormone.nutrients-10-00652-t001_Table 1Table 1Published studies on the impact of vitamin D on vascular calcification (VC).Aspect of Vitamin D ExaminedStudy ModelProposed Mechanisms for VCReference No.HypervitaminosisIn

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