Evidence map›Paper›PMID 21693169›Full record

ReviewMolecular and cellular endocrinology2011

The role of vitamin D receptor mutations in the development of alopecia.

Peter J Malloy, David Feldman

Registry-linked trialAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03154528 (Role of Vitamin D in Androgenetic Alopecia), which is not on this map. Cited by 40 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT03154528 unknown statusnot on this mapstarted 2019, after this paper: background citation

Role of Vitamin D in Androgenetic Alopecia

TypeobservationalSponsorAssiut UniversityRan2019 to 2019Enrolled90ConditionsAlopecia, AndrogeneticArmsserum vitamin D level by ELISA
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 3 syntheses or guidelines pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Tru9I Variant as a Novel Genetic Marker for Vitamin D Deficiency in Alopecia Areata.Clinical, cosmetic and investigational dermatology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Current issues in molecular biology · 2023
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Genetics of Refractory Rickets: Identification of NovelJournal of pediatric genetics · 2018
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Peter J MalloyStanford University School of Medicine, Stanford, CA 94305-5103, USA.
David Feldman
Stanford University · US

Funding

VITAMIN D RECEPTOR AND REGULATION OF HORMONE RESPONSER01DK042482 · NIDDK · STANFORD UNIVERSITY · PI FELDMAN, DAVID · 1991 to 2010
$3.1M
VITAMIN D RECEPTOR AND REGULATION OF HORMONE RESPONSER56DK042482 · NIDDK · STANFORD UNIVERSITY · PI FELDMAN, DAVID · 2005 to 2005
$115k
NIDDK NIH HHS DK042482NIDDK NIH HHS R01 DK042482
6 · The paper itself

Abstract

Hereditary Vitamin D Resistant Rickets (HVDRR) is a rare disease caused by mutations in the vitamin D receptor (VDR). The consequence of defective VDR is the inability to absorb calcium normally in the intestine. This leads to a constellation of metabolic abnormalities including hypocalcemia, secondary hyperparathyroidism and hypophosphatemia that cause the development of rickets at an early age in affected children. An interesting additional abnormality is the presence of alopecia in some children depending on the nature of the VDR mutation. The data indicate that VDR mutations that cause defects in DNA binding, RXR heterodimerization or absence of the VDR cause alopecia while mutations that alter VDR affinity for 1,25(OH)(2)D(3) or disrupt coactivator interactions do not cause alopecia. The cumulative findings indicate that hair follicle cycling is dependent on unliganded actions of the VDR. Further research is ongoing to elucidate the role of the VDR in hair growth and differentiation.

Indexed as

Mutation25-Hydroxyvitamin D3 1-alpha-HydroxylaseAlopeciaAnimalsCalciumFamilial Hypophosphatemic RicketsHair FollicleHomeostasisHumansMiceMice, KnockoutReceptors, CalcitriolTranscription Factors25-Hydroxyvitamin D3 1-alpha-HydroxylaseCalciumHR protein, humanReceptors, CalcitriolTranscription Factors

Identifiers

PMID21693169
PMCPMC3196847
OpenAlexW2152794908

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.