Vitamin D and Bone: A Story of Endocrine and Auto/Paracrine Action in Osteoblasts.
Level 5 - mechanism / opinion, no new human data
Narrative review of cellular and molecular mechanisms without primary human data
PubMed 36771187 · doi:10.3390/nu15030480
What was done
This narrative review synthesizes evidence on the cellular and molecular mechanisms by which 1α,25-dihydroxyvitamin D3 (1α,25-OH2D3) acts via vitamin D receptors to regulate osteoblast proliferation, apoptosis, differentiation, and bone matrix mineralization, as well as the role of local vitamin D metabolic machinery.
What was found
The abstract reports no numerical findings. Qualitatively, it reports that osteoblast gene transcription responses to vitamin D depend on the differentiation and mineralization stage, and that osteoblasts express functional 1α-hydroxylase (CYP27B1) for local 1α,25-OH2D3 synthesis and 24-hydroxylase (CYP24A1) for its degradation, demonstrating autocrine/paracrine regulation of bone formation.
Why it matters
This work summarizes the conceptual shift in bone biology from viewing vitamin D solely as a classic renal endocrine hormone to recognizing its locally produced autocrine and paracrine actions directly within bone-forming cells.
Limits
The abstract describes a narrative review with no primary empirical data, no systematic review methodology, and no human clinical outcome metrics. Detailed sample sizes, study designs of cited literature, and quantitative effect sizes cannot be evaluated from the abstract alone.
Cited by
- supports Vitamin D binding to osteoblasts stimulates bone formation.