2019
DOI: 10.1002/jbmr.3884
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Vitamin D Metabolism Revised: Fall of Dogmas

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Cited by 76 publications
(53 citation statements)
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References 115 publications
(181 reference statements)
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“…Macrophages' CYP27B1 is stimulated by interferon-γ (INFγ), tumor necrosis factor α (TNFα), interleukin (IL) 1, 2 and 15, but not by PTH. Moreover, dexamethasone inhibits CYP27B1 [55]. In addition to macrophages, also dendritic cells (DC), Th lymphocytes and B lymphocytes express CYP27B1, but only when they are activated.…”
Section: (Oh) 2 D and The Case For Vitamin D Immunobiologymentioning
confidence: 99%
See 1 more Smart Citation
“…Macrophages' CYP27B1 is stimulated by interferon-γ (INFγ), tumor necrosis factor α (TNFα), interleukin (IL) 1, 2 and 15, but not by PTH. Moreover, dexamethasone inhibits CYP27B1 [55]. In addition to macrophages, also dendritic cells (DC), Th lymphocytes and B lymphocytes express CYP27B1, but only when they are activated.…”
Section: (Oh) 2 D and The Case For Vitamin D Immunobiologymentioning
confidence: 99%
“…In these cells 1,25(OH) 2 D functions as a 1αhydroxylase inhibitor, thus controlling their activation and proliferation. As described further in details in paragraph 6, 1,25(OH) 2 D exerts many autocrine and paracrine functions on immune system cells, ensuring a feedback control on immune cells themselves [55]. Beyond classical renal CYP27B1 modulation, the novelty in the field is represented by a completely different regulation of CYP27B1 in the other tissues, particularly in the immune system.…”
Section: (Oh) 2 D and The Case For Vitamin D Immunobiologymentioning
confidence: 99%
“…Correction of vitamin D deficiency is relatively easy by either increased exposure to sunlight (unlikely for patients with ARDS), oral or parental vitamin D supplementation, or supplementation with 25OHD (calcifediol). To correct vitamin D deficiency in severely sick patients much higher doses than usual are needed [81], probably related to impaired hepatic conversion of vitamin D into 25OHD [82]. Calcifediol may have some advantages over the native vitamin D: it has a more reliable intestinal absorption (close to 100 %) and can rapidly restore serum concentrations of 25OHD as it does not require hepatic 25-hydroxylation.…”
Section: Clinical Consequences: Vitamin D Status and Adrs During Coromentioning
confidence: 99%
“…VDR is expressed in more than 30 target tissues in humans [11], and a genome-wide analysis revealed more than 1000 VDR-specific genomic binding sites in most tissues, suggesting that the transcriptionally active form of vitamin D influences the expression of many genes likely to be relevant for human health and disease [12]. Furthermore, lessons from VDR and CYP27B1 null mice indicate that VDR may act either dependently or independently of 1,25(OH) 2 D. Thus, multiple receptors and ligands may participate in the vitamin D endocrine system [1,3,13], in addition to non-genomic actions via unclear mechanisms [14][15][16]. Indeed, consistent with the multiple biological functions of the active form of vitamin D, there is evidence that VDR, which is normally localized in the nucleus and associated with gene transcription, may also be present in the plasma membrane and mediate rapid responses to 1,25(OH) 2 D [11,17].…”
Section: Sources Metabolism and Pleiotropic Functions Of Vitamin Dmentioning
confidence: 99%