Evidence map›Paper›PMID 25755727›Full record

ArticleInternational journal of clinical and experimental pathology2015

Genistein attenuates glucocorticoid-induced bone deleterious effects through regulation Eph/ephrin expression in aged mice.

Yuan Cheng, Wei-Lin Wang, Jun-Jun Liang

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Preventive effects ofExperimental and therapeutic medicine · 2017
    Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Yuan ChengDepartment of Endocrinology, The Second Affiliated Hospital of Anhui Medical University 678 Furong Road, Hefei 230601, China.
Wei-Lin Wang2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, The Key Laboratory of Hormones and Development (Ministry of Health), Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University 66 Tongan Road, Tianjin 300070, China.
Jun-Jun LiangDepartment of Neurosurgery, The People's Hospital of Anqiu 246 Jiankang Road, Weifang 262100, China.
Anhui Medical University · CNTianjin Medical University · CNWeifang People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study was performed to investigate bone deteriorations and the involvement of skeletal Eph/ephrin signaling pathway of GIOP aged mice in response to the treatment of genistein.

methodsThe biomarkers in serum and urine were measured, tibias were taken for the measurement on gene and protein expression and histomorphology analysis, and femurs were taken for the measurement on bone Ca and three-dimensional architecture of trabecular bone.

resultsGenistein showed a greater increase in bone Ca, BMD and significantly increased FGF-23 and OCN, reduced TRACP-5b, PTH and CTX in GIOP mice. Genistein reversed DXM-induced trabecular deleterious effects and stimulated bone remodeling. The treatment of DXM group with genistein significantly elevated the ratio of OPG/RANKL. Moreover, genistein administration down-regulated the mRNA and protein expression of Eph A2 and ephrin A2 in tibia of the GIOP mice. In contrast, the mRNA and protein expression of Eph B4 and ephrin B2 were increased in mice treated by DXM with genistein as compared to the DXM single treatment.

conclusionsDXM-induced trabecular bone micro-structure deterioration in aged mice was involved in the regulation of the Eph receptors and ephrin ligands. Genistein might represent a therapy with bone-forming as well as an anti-resorptive activity in GIOP mice. The underlying mechanism was mediated, at least partially, through regulation Eph/ephrin signaling.

Indexed as

AnimalsBlotting, WesternBone and BonesBone DensityDexamethasoneEphrinsFemaleFibroblast Growth Factor-23GenisteinGlucocorticoidsHumansMaleMiceMice, Inbred C57BLProtein Kinase InhibitorsReceptors, Eph FamilyDexamethasoneEphrinsFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23GenisteinGlucocorticoidsProtein Kinase InhibitorsReceptors, Eph FamilybonedexamethasoneEph/ephringenistein

Identifiers

PMID25755727
PMCPMC4348890
OpenAlexW77991184

What OpenQuestion holds

Textmetadata
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.