Evidence map›Paper›PMID 27533615›Full record

ReviewArchives of endocrinology and metabolism2016

Genetics of osteoporosis: searching for candidate genes for bone fragility.

Manuela G M Rocha-Braz, Bruno Ferraz-de-Souza

Registry-linked trialOpen access · diamondAbstract readReview
In one paragraph

Review in Archives of endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04856683 (PRecisiOn MEdicine to Target Frailty of Endocrine-metabolic Origin), which is not on this map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.1field-weighted citation impact, top 5% 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.

NCT04856683 unknown statusnot on this mapstarted 2020, after this paper: background citation

PRecisiOn MEdicine to Target Frailty of Endocrine-metabolic Origin

TypeobservationalSponsorUniversity of Roma La SapienzaRan2020 to 2024Enrolled1,100ConditionsFrailty
3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Plastin 3 in health and disease: a matter of balance.Cellular and molecular life sciences : CMLS · 2021
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. A novel dominant COL11A1 mutation in a child with Stickler syndrome type II is associated with recurrent fractures.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2018
    Article
  18. [Gut microbiota and osteoporosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2016
    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 2 institutions in 1 country.

Manuela G M Rocha-BrazDivisão de Endocrinologia e Laboratório de Investigação Médica 18 (LIM-18), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HCFMUSP), São Paulo, SP, Brasil.
Bruno Ferraz-de-SouzaDivisão de Endocrinologia e Laboratório de Investigação Médica 18 (LIM-18), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HCFMUSP), São Paulo, SP, Brasil.
Irmandade da Santa Casa de Misericórdia de São Paulo · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of osteoporosis, a common disease with great morbidity and mortality, comprises environmental and genetic factors. As with other complex disorders, the genetic basis of osteoporosis has been difficult to identify. Nevertheless, several approaches have been undertaken in the past decades in order to identify candidate genes for bone fragility, including the study of rare monogenic syndromes with striking bone phenotypes (e.g. osteogenesis imperfecta and osteopetroses), the analysis of individuals or families with extreme osteoporotic phenotypes (e.g. idiopathic juvenile and pregnancy-related osteoporosis), and, chiefly, genome-wide association studies (GWAS) in large populations. Altogether, these efforts have greatly increased the understanding of molecular mechanisms behind bone remodelling, which has rapidly translated into the development of novel therapeutic strategies, exemplified by the tales of cathepsin K (CTSK) and sclerostin (SOST). Additional biological evidence of involvement in bone physiology still lacks for several candidate genes arisen from GWAS, opening an opportunity for the discovery of new mechanisms regulating bone strength, particularly with the advent of high-throughput genomic technologies. In this review, candidate genes for bone fragility will be presented in comprehensive tables and discussed with regard to how their association with osteoporosis emerged, highlighting key players such as LRP5, WNT1 and PLS3. Current limitations in our understanding of the genetic contribution to osteoporosis, such as yet unidentified genetic modifiers, may be overcome in the near future with better genotypic and phenotypic characterisation of large populations and the detailed study of candidate genes in informative individuals with marked phenotype.

Indexed as

MutationBone DensityFemaleGenome-Wide Association StudyHumansMaleOsteoporosisRisk FactorsWnt Signaling Pathway

Identifiers

PMID27533615
PMCPMC10118722
OpenAlexW2517977395

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.