ReviewiScience2026
Vitamin D as a cellular endocrine system: Tissue-specific microcircuits, immune reprogramming, and metabolic resistance.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circulating 25-hydroxyvitamin D is the standard marker of vitamin D status, but tissue responses to vitamin D vary across organs, inflammatory states, and clinical settings. This review frames vitamin D biology as a cellular endocrine system in which substrate transport, local CYP27B1-mediated activation, CYP24A1-mediated inactivation, and VDR responsiveness form tissue-specific microcircuits. Evidence from barrier epithelia, immune cells, and brain-resident cells indicates that megalin/cubilin-dependent uptake, local enzyme balance, redox state, and downstream transcriptional competence can decouple serum 25-hydroxyvitamin D from intracellular vitamin D activity. We use metabolic vitamin D resistance to describe acquired low-responsiveness states driven by inflammation, aging, redox stress, or chronic disease. This framework clarifies biomarker interpretation and supports more context-aware approaches to supplementation, trial design, and tissue-targeted intervention.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.