Evidence map›Paper›PMID 35879773›Full record

ReviewCell communication and signaling : CCS2022

STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis.

Xiaoli Hou, Faming Tian

Open access · goldAbstract readReviewVideo-Audio Media
In one paragraph

Review in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. How I Treat: STAT3 hyper IgE syndrome.Journal of human immunity · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Loss of Stat3 in Prx1Advanced biology · 2025
    Article
  17. Article
  18. Article
  19. International journal of molecular sciences · 2025
    Article
  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

2 authors at 1 institution in 1 country.

Xiaoli HouSchool of Public Health, North China University of Science and Technology, Caofeidian Dis, Bohai Road 21, Tangshan, 063210, People's Republic of China.
Faming TianSchool of Public Health, North China University of Science and Technology, Caofeidian Dis, Bohai Road 21, Tangshan, 063210, People's Republic of China. tfm9911316@163.com.
North China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is a common skeletal disease with marked bone loss, deterioration of the bone microstructure and bone fragility. An abnormal bone remodelling cycle with relatively increased bone resorption is the crucial pathophysiological mechanism. Bone remodelling is predominantly controlled by osteoblasts and osteoclasts, which are specialized cell types that are regulated by a variety of osteogenic and osteoclastic factors, including cytokines expressed within the bone microenvironment under local or systemic inflammatory conditions. Signal transducer and activator of transcription 3 (STAT3) plays a prominent role in the communication between cytokines and kinases by binding downstream gene promotors and is involved in a wide range of biological or pathological processes. Emerging evidence suggests that STAT3 and its network participate in bone remodelling and the development of osteoporosis, and this factor may be a potent target for osteoporosis treatment. This review focuses on the role and molecular mechanism of the STAT3 signalling pathway in osteogenesis, osteoclastogenesis and osteoporosis, particularly the bone-related cytokines that regulate the osteoblastic differentiation of bone marrow stromal cells and the osteoclastic differentiation of bone marrow macrophages by initiating STAT3 signalling. This review also examines the cellular interactions among immune cells, haematopoietic cells and osteoblastic/osteoclastic cells. Video abstract.

Indexed as

Bone ResorptionOsteoporosisCell DifferentiationCytokinesHumansOsteoblastsOsteoclastsOsteogenesisRANK LigandSTAT3 Transcription FactorCytokinesRANK LigandSTAT3 protein, humanSTAT3 Transcription FactorOsteoclastogenesisOsteogenesisOsteoporosisSTAT3

Identifiers

PMID35879773
PMCPMC9310501
OpenAlexW4287147347

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.