Evidence map›Paper›PMID 36881265›Full record

ReviewCurrent osteoporosis reports2023

SP7: from Bone Development to Skeletal Disease.

Jialiang S Wang, Nicha Tokavanich, Marc N Wein

Open access · greenAbstract readReview
In one paragraph

Review in Current osteoporosis reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.7field-weighted citation impact, top 7% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Modulation of the gut-bone axis:Frontiers in immunology · 2025
    Article
  10. Regulation of Skeletal Development and Maintenance by Runx2 and Sp7.International journal of molecular sciences · 2024
    Review
  11. Article
  12. American journal of translational research · 2024
    Article
  13. Review
  14. Article
  15. Metabolic regulation by biomaterials in osteoblast.Frontiers in bioengineering and biotechnology · 2023
    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

3 authors at 2 institutions in 1 country.

Jialiang S WangEndocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. jwang101@mgh.harvard.edu.ORCID http://orcid.org/0000-0002-3409-7619
Nicha TokavanichEndocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Marc N WeinEndocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Harvard University · USBroad Institute · US

Funding

Tissue Phenotyping CoreP01DK011794 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MANNSTADT, MICHAEL · 1986 to 2023
$44.4M
TRAINING PROGRAM IN ENDOCRINOLOGY AND DIABETEST32DK007028 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Karen K Miller · 1986 to 2026
$18.5M
The role of salt inducible kinases in parathyroid hormone action in boneR01DK116716 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Marc Nathan Wein · 2018 to 2026
$3.8M
Comprehensive investigation of SP7 during the osteoblast-to-osteocyte transitionK99AR081897 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI WANG, JIALIANG · 2023 to 2024
$186k
NIAMS NIH HHS K99 AR081897NIDDK NIH HHS P01 DK011794NIDDK NIH HHS R01 DK116716NIDDK NIH HHS T32 DK007028
6 · The paper itself

Abstract

purpose of reviewThe purpose of this review is to summarize the different roles of the transcription factor SP7 in regulating bone formation and remodeling, discuss current studies in investigating the causal relationship between SP7 mutations and human skeletal disease, and highlight potential therapeutic treatments that targeting SP7 and the gene networks that it controls. RECENT

findingsCell-type and stage-specific functions of SP7 have been identified during bone formation and remodeling. Normal bone development regulated by SP7 is strongly associated with human bone health. Dysfunction of SP7 results in common or rare skeletal diseases, including osteoporosis and osteogenesis imperfecta with different inheritance patterns. SP7-associated signaling pathways, SP7-dependent target genes, and epigenetic regulations of SP7 serve as new therapeutic targets in the treatment of skeletal disorders. This review addresses the importance of SP7-regulated bone development in studying bone health and skeletal disease. Recent advances in whole genome and exome sequencing, GWAS, multi-omics, and CRISPR-mediated activation and inhibition have provided the approaches to investigate the gene-regulatory networks controlled by SP7 in bone and the therapeutic targets to treat skeletal disease.

Indexed as

OsteogenesisOsteogenesis ImperfectaBone and BonesHumansMutationSignal TransductionSp7 Transcription FactorSP7 protein, humanSp7 Transcription FactorBone developmentSkeletal diseaseSP7Therapeutic approaches

Identifiers

PMID36881265
PMCPMC10758296
OpenAlexW4323348632

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.