Evidence map›Paper›PMID 31440530›Full record

ArticleBone reports2019

Stat3 in osteocytes mediates osteogenic response to loading.

Kylie A Corry, Hongkang Zhou, Tatiana Brustovetsky, Evan R Himes, Nicoletta Bivi, M Ryne Horn, Yukiko Kitase, Joseph M Wallace, Teresita Bellido, Nickolay Brustovetsky and 1 more

Open access · goldAbstract read
In one paragraph

Article in Bone reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  4. Review
  5. In Silico Investigation RevealsMedical sciences (Basel, Switzerland) · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Exercise maintains bone homeostasis by promoting osteogenesis through STAT3.International journal of biological sciences · 2023
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Review
  20. 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

11 authors at 3 institutions in 1 country.

Kylie A CorryDepartment of Biology, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Hongkang ZhouDepartment of Biology, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Tatiana BrustovetskyDepartment of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Evan R HimesDepartment of Biology, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Nicoletta BiviDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
M Ryne HornDepartment of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Yukiko KitaseDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Joseph M WallaceDepartment of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Teresita BellidoDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Nickolay BrustovetskyDepartment of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Jiliang LiDepartment of Biology, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
University of Indianapolis · USIndiana University School of MedicineRichard L. Roudebush VA Medical Center · US

Funding

CRMP2, mitochondria, and Huntington’s diseaseR01NS098772 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI BRUSTOVETSKY, NICKOLAY, KHANNA, RAJESH · 2017 to 2021
$2.8M
NINDS NIH HHS R01 NS098772
6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (Stat3) is a member of the Stat family of proteins involved in signaling in many different cell types, including osteocytes. Osteocytes are considered major mechanosensing cells in bone due to their intricate dendritic networks able to sense changes in physical force and to orchestrate the response of osteoclasts and osteoblasts. We examined the role of Stat3 in osteocytes by generating mice lacking Stat3 in these cells using the Dmp-1(8kb)-Cre promoter (Stat3cKO mice). Compared to age-matched littermate controls, Stat3cKO mice of either sex (18 weeks old) exhibit reduced bone formation indices, decreased osteoblasts and increased osteoclasts, and altered material properties, without detectable changes in bone mineral density (BMD) or content of either trabecular or cortical bone. In addition, Stat3cKO mice of either sex show significantly decreased load-induced bone formation. Furthermore, pharmacologic inhibition of Stat3 in osteocytes

Indexed as

ATPBone formationMechanotransductionOsteocyteROSSignal transducers and activators of transcription 3 (Stat3)

Identifiers

PMID31440530
PMCPMC6700265
OpenAlexW2966582885

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.