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home:pathogenesis:vitamind:mechanisms [01.25.2019] – [Recent research] sallieq | home:pathogenesis:vitamind:mechanisms [09.14.2022] (current) – external edit 127.0.0.1 | ||
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Given that the VDR is fundamentally a control system for the innate immune response, the body upregulates the Receptor' | Given that the VDR is fundamentally a control system for the innate immune response, the body upregulates the Receptor' | ||
- | One such mechanism is the CYP27B1 pathway.(({{pubmed> | + | One such mechanism is the CYP27B1 pathway.(({{pmid> |
< | < | ||
- | **//C.D. Nelson//** (({{pubmed> | + | **//C.D. Nelson//** (({{pmid> |
===== Elevated 1,25-D for extended periods implies a partially blocked VDR ===== | ===== Elevated 1,25-D for extended periods implies a partially blocked VDR ===== | ||
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===== Effects of VDR blockage on CYP24A1, an enzyme regulating conversion of 25-D into 1,25-D ===== | ===== Effects of VDR blockage on CYP24A1, an enzyme regulating conversion of 25-D into 1,25-D ===== | ||
- | When active, the VDR transcribes CYP24A1 (sometimes referred to as CYP24), which regulates levels of 25-D and 1,25-D. CYP24A1 breaks down excess 1,25-D, ensuring that the level of 1,25-D in the body stays in the normal range.(({{pubmed> | + | When active, the VDR transcribes CYP24A1 (sometimes referred to as CYP24), which regulates levels of 25-D and 1,25-D. CYP24A1 breaks down excess 1,25-D, ensuring that the level of 1,25-D in the body stays in the normal range.(({{pmid> |
< | < | ||
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===== Effects of VDR blockage on the PXR, a receptor which converts pre-vitamin D into 25-D ===== | ===== Effects of VDR blockage on the PXR, a receptor which converts pre-vitamin D into 25-D ===== | ||
- | When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop via the CYP27A1 pathway.(({{pubmed> | + | When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop via the CYP27A1 pathway.(({{pmid> |
This mechanism works well when 1,25-D is within normal ranges. But when 1,25-D becomes extremely high, as in the case of chronic diseases, 25-D is downregulated to abnormally low levels, leading some observers to erroneously conclude that vitamin D deficiency causes disease. | This mechanism works well when 1,25-D is within normal ranges. But when 1,25-D becomes extremely high, as in the case of chronic diseases, 25-D is downregulated to abnormally low levels, leading some observers to erroneously conclude that vitamin D deficiency causes disease. | ||
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===== Recent research ===== | ===== Recent research ===== | ||
- | We evaluated whether the ability of M. leprae to induce type I IFN blocks the intrinsic activation of the vitamin D pathway, representing an escape mechanism by which the bacterium evades the host response. | + | We evaluated whether the ability of M. leprae to induce type I IFN blocks the intrinsic activation of the vitamin D pathway, representing an escape mechanism by which the bacterium evades the host response. |
< | < | ||
- | </ | + | </ |
===== Related publications and presentations ===== | ===== Related publications and presentations ===== | ||
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{{tag> | {{tag> | ||
+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
- | (({{pubmed> | + | (({{pmid> |
* Legacy content | * Legacy content | ||
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The progressive decline in kidney function and concomitant loss of renal 1α-hydroxylase (CYP27B1) in chronic kidney disease (CKD) are associated with a gradual loss of circulating 25-hydroxyvitamin D3 (25(OH)D3) and 1α, | The progressive decline in kidney function and concomitant loss of renal 1α-hydroxylase (CYP27B1) in chronic kidney disease (CKD) are associated with a gradual loss of circulating 25-hydroxyvitamin D3 (25(OH)D3) and 1α, | ||
- | ===== References ===== | + | ===== References =====</ |