Evidence map›Paper›PMID 33888646›Full record

ArticleAging2021

Low magnitude vibration alleviates age-related bone loss by inhibiting cell senescence of osteogenic cells in naturally senescent rats.

Jirui Wen, Mingyue Bao, Min Tang, Xueling He, Xinghong Yao, Liang Li

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Consequences of Aging on Bone.Aging and disease · 2023
    Pooled it
  2. Review
  3. Review
  4. Review
  5. SIRT1 and exercise-induced bone metabolism: a regulatory nexus.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
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

6 authors at 2 institutions in 1 country.

Jirui WenInstitute of Biomedical Engineering, West China School of Basic Medical Science and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China.
Mingyue BaoInstitute of Biomedical Engineering, West China School of Basic Medical Science and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China.
Min TangInstitute of Biomedical Engineering, West China School of Basic Medical Science and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China.
Xueling HeLaboratory Animal Center, Sichuan University, Chengdu 610041, Sichuan, China.
Xinghong YaoInstitute of Biomedical Engineering, West China School of Basic Medical Science and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China.
Liang LiInstitute of Biomedical Engineering, West China School of Basic Medical Science and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China.
West China Medical Center of Sichuan University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunction of bone marrow mesenchymal stem cells (BMSCs), osteoblasts and osteocytes may be one of the main causes of bone loss in the elderly. In the present study, we found osteogenic cells from aged rats all exhibited senescence changes, with the most pronounced senescence changes in osteocytes. Meanwhile, the proliferative capacity and functional activity of osteogenic cells from aged rats were suppressed. Osteogenic differentiation capacity of BMSCs from aged rats decreased while adipogenic capacity increased. The mineralization capacity, ALP activity and osteogenic proteins expression of osteoblasts from aged rats decreased. Additionally, osteocytes from aged rats up-expressed sclerosteosis protein, a negative regulator of bone formation. To inhibit osteogenic cell senescence, we use low magnitude vibration (LMV) to eliminate the senescent osteogenic cells. After LMV treatment, the number of osteogenic cells staining positively for senescence-associated-β-galactosidase (SA-β-Gal) decreased significantly. Besides, the expression of anti-aging protein SIRT1 was upregulated significantly, while p53 and p21 were downregulated significantly after LMV treatment. Thus, the LMV can inhibit the senescence of osteogenic cells partly through the Sirt1/p53/p21 axis. Furthermore, LMV was found to promote bone formation of aged rats. These results suggest that the inhibition of osteogenic cell senescence by LMV is a valuable treatment to prevent or delay osteoporosis.

Indexed as

AnimalsCells, CulturedCellular SenescenceCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalDown-RegulationFemaleHumansMaleMesenchymal Stem CellsOsteoblastsOsteogenesisOsteoporosisPrimary Cell CultureRatsSirtuin 1Cdkn1a protein, ratCyclin-Dependent Kinase Inhibitor p21Sirt1 protein, ratSirtuin 1Tp53 protein, ratTumor Suppressor Protein p53low magnitude vibrationosteogenesisosteoporosissenescence

Identifiers

PMID33888646
PMCPMC8109117
OpenAlexW3155933741

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.