Ask about this productRelated genes to: CYP24A1 antibody
- Gene:
- CYP24A1 NIH gene
- Name:
- cytochrome P450 family 24 subfamily A member 1
- Previous symbol:
- CYP24
- Synonyms:
- CP24, P450-CC24
- Chromosome:
- 20q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-09
- Date modifiied:
- 2018-02-28
Related products to: CYP24A1 antibody
Related articles to: CYP24A1 antibody
- Hypercalcemia in infancy is rare and often presents with nonspecific clinical signs, making early recognition challenging. This report describes two infants with severe symptomatic hypercalcemia due to distinct etiologies and highlights the diagnostic value of sterile pyuria as an early clinical clue. - Source: PubMed
Publication date: 2026/03/30
Ahel Ivona ButoracAndritsos VerenikiKošuljandić ĐurđicaSeverinski SrećkoJešić MajaGrozdanić Kristina LovrinovićDekanić Kristina BarabaJambrović JuricaČače Iva Bilić - Calcium (Ca²⁺) homeostasis is tightly regulated by the coordinated actions of the intestine, kidneys and bone. Ca²⁺ transport occurs via either a paracellular pathway, which depends on the expression of select claudins, including claudin-12 (CLDN12) in the tight junction, or a transcellular pathway, involving apical influx through TRPV6. While disruption of paracellular or transcellular pathways impairs transepithelial Ca²⁺ flux, Cldn12-deficient mice and Trpv6 mutant (Trpv6) mice do not display alterations in Ca²⁺ balance as reported previously, perhaps because one pathway compensates for the other. To test this hypothesis, we generated a double knockout mouse (DKO, Cldn12/ Trpv6) to assess Ca²⁺ homeostasis using metabolic cage balance studies, quantitative real-time PCR, and micro-computed tomography (Micro-CT). Despite lacking these key Ca²⁺ transport mechanisms, DKO mice maintained normal blood Ca²⁺. However, PTH and calcitriol were significantly elevated, as were renal Cyp27b1 and Cyp24a1 expression, consistent with hormonal compensation. The proximal colon and cecum exhibited significant compensatory changes in Ca²⁺-regulatory gene expression, including upregulation of the Ca²⁺ buffer S100g and basolateral extrusion mechanism Atp2b1. Notably, the Ca²⁺ channel Trpv5, which is absent from the intestine, became detectable in the proximal colon and cecum, but not in the distal colon or small intestine of DKO mice. Micro-CT of bone revealed reduced trabecular bone volume and thickness, indicating increased bone resorption as a secondary compensatory mechanism. This study highlights the adaptive plasticity of Ca²⁺-regulatory mechanisms and suggests a role for TRPV5 in reabsorbing Ca²⁺ from the proximal colon and cecum when upstream mechanisms of Ca²⁺ absorption are impaired. - Source: PubMed
Publication date: 2026/04/09
Deluque Amanda LimaPan WanlingO'Neill DeborahBogdanovic MilosDimke HenrikDoschak Michael RAlexander R Todd - Despite compelling epidemiological evidence linking vitamin D deficiency to adverse outcomes in chronic obstructive pulmonary disease (COPD), asthma, and cystic fibrosis, randomized controlled trials have consistently failed to demonstrate clinically meaningful benefits from oral vitamin D supplementation. This disconnect between observational associations and interventional evidence represents a significant paradox in pulmonary medicine. Recent meta-analyses have found limited protective or therapeutic effects of oral supplementation on exacerbation rates, lung function, hospitalizations, or quality of life measures. We propose that this therapeutic failure reflects not a lack of vitamin D's efficacy but rather a fundamental limitation in the route of delivery. Oral vitamin D supplementation undergoes hepatic metabolism and systemic dilution before reaching respiratory tissues. High expression of CYP24A1, the vitamin D-inactivating enzyme, in pulmonary vasculature suggests that orally delivered vitamin D may be degraded before reaching the lung lumen. The respiratory epithelium possesses complete machinery for vitamin D activation, and vitamin D receptors are expressed throughout airway epithelial and immune cells, making direct pulmonary delivery mechanistically feasible. Pre-clinical studies demonstrate that nebulized or inhaled vitamin D reduces inflammation, protects epithelial barrier function, and improves lung function in murine models of respiratory disease without producing off-target systemic effects or hypercalcemia. Direct lung delivery of vitamin D represents an unexplored therapeutic strategy that could transform management of chronic respiratory diseases, like COPD, by achieving local therapeutic concentrations while minimizing systemic exposure. Clinical trials investigating safety, dosing optimization, and efficacy are warranted. - Source: PubMed
Publication date: 2026/03/31
Schichlein Kevin DJaspers IlonaDrummond M Bradley - Vitamin D is a group of fat-soluble vitamins that plays critical roles in calcium-phosphate homeostasis, bone health, and immune regulation. The metabolic pathway of vitamin D involves two key enzymatic steps: hepatic 25-hydroxylation to produce 25-hydroxyvitamin D [25(OH)D] and renal 1α-hydroxylation to generate the biologically active form 1,25-dihydroxyvitamin D [1,25(OH)D]. 25(OH)D serves as the gold standard biomarker for assessing vitamin D status due to its high circulating concentration, long half-life, and stable levels. This metabolic process is precisely regulated by parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and negative feedback mechanisms mediated by the vitamin D receptor (VDR). Recent studies have demonstrated that CYP27B1, the gene encoding 1α-hydroxylase, is also widely expressed in extrarenal tissues including prostate, breast, placenta, and macrophages, suggesting important roles for vitamin D in local paracrine and autocrine regulation. Dysregulation of vitamin D metabolism is closely associated with the pathogenesis of various diseases, including vitamin D-dependent rickets type 1A (VDDR-1A), chronic kidney disease-mineral and bone disorder (CKD-MBD), tumor-induced osteomalacia (TIO), granulomatous diseases, and CYP24A1 deficiency-related hypercalcemia. Notably, 24,25-dihydroxyvitamin D [24,25(OH)D], traditionally considered an inactive metabolic end-product, may possess independent biological functions, and its ratio to 1,25(OH)D can serve as a novel biomarker for assessing vitamin D metabolic status. This review systematically examines the metabolic pathways and regulatory mechanisms of vitamin D, elucidates their associations with disease pathogenesis, and provides theoretical foundation for personalized clinical diagnosis and precision therapy. Future research should establish standardized multi-parameter detection protocols to advance the clinical application of vitamin D metabolomics in precision medicine. - Source: PubMed
Publication date: 2026/03/18
Ji YumengBi RuruWang Lin - We hypothesized that vitamin D3 (VD3) coordinates a complex functional interplay between cerebral homeostasis and skeletal integrity by modulating mineral metabolism and osteotropic signaling. This neuroskeletal axis is likely mediated via a feedback loop involving fibroblast growth factor 23 (FGF23), a key regulator within both osseous and cerebral tissues. In this context, our study aimed to characterize tissue-specific adaptive responses by analyzing correlations between components of the vitamin D3 system and FGF23 signaling under physiological and VD3-deficient conditions. - Source: PubMed
Shymanskyi ILisakovska OKhomenko ABilous VKucheriavyi YPoladych IParkhomenko YVeliky M