Evidence map›Paper›PMID 34136574›Full record

ArticleBioMed research international2021

Inhibition of SDF-1/CXCR4 Axis to Alleviate Abnormal Bone Formation and Angiogenesis Could Improve the Subchondral Bone Microenvironment in Osteoarthritis.

Hanjun Qin, Xingqi Zhao, Yan Jun Hu, Shengnan Wang, Yunfei Ma, Siying He, Ke Shen, Haoyang Wan, Zhuang Cui, Bin Yu

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.6field-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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Synovitis Ointment Improved Knee Osteoarthritis by Suppressing SDF-1/CXCR4 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  18. 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

10 authors at 1 institution in 1 country.

Hanjun QinDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID https://orcid.org/0000-0002-9982-6157
Xingqi ZhaoDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yan Jun HuDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Shengnan WangDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yunfei MaDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Siying HeDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Ke ShenDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Haoyang WanDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zhuang CuiDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID https://orcid.org/0000-0002-1061-0190
Bin YuDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID https://orcid.org/0000-0002-3109-2062
Nanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of the osteoarthritis (OA) is complex. Abnormal subchondral bone metabolism is an important cause of this disease. Further understanding on the pathology of the subchondral bone in OA may provide a new therapy. This research is about to investigate the role of SDF-1 in the subchondral bone during the pathological process of OA. In vitro, Transwell was used to test the migratory ability of bone marrow mesenchymal stem cells (BMSCs) and human umbilical vein endothelial cells (HUVECs). Western blot presented the protein level after SDF-1 treatment in BMSCs and HUVESs. Alizarin red was used to assess the ability of osteogenic differentiation. To inhibit SDF-1 signaling pathway in vivo, AMD3100 (SDF-1 receptor blocker) was continuously delivered via miniosmotic pump for 4 weeks in mice after performing anterior cruciate ligament transaction surgery. Micro-CT, histology staining, immunofluorescence, immunohistochemistry, and TRAP staining were used to assess the role of SDF-1 on osteogenesis and angiogenesis in the subchondral bone. Our results showed that SDF-1 could recruit BMSCs, activate the p-ERK pathway, and enhance osteogenic differentiation. SDF-1 promoted the ability of proliferation, migration and tube formation of HUVECs by activating the ERK and AKT signaling pathways. In an animal study, inhibition of SDF-1/CXCR4 axis could significantly reduce subchondral osteogenesis differentiation and H-type vessel formation. Furthermore, the AMD3100-treated group showed less cartilage destruction and bone resorption. Our research shows that SDF-1 alters the microenvironment of the subchondral bone by promoting osteoid islet formation and abnormal H-type angiogenesis in the subchondral bone, resulting in articular cartilage degeneration.

Indexed as

Neovascularization, PathologicAnimalsBone and BonesBone ResorptionCartilageCartilage, ArticularCell MovementCell ProliferationChemokine CXCL12Extracellular Signal-Regulated MAP KinasesFemurHumansHuman Umbilical Vein Endothelial CellsMaleMesenchymal Stem CellsMiceChemokine CXCL12CXCL12 protein, humanCxcl12 protein, mouseCXCR4 protein, humanCXCR4 protein, mouseExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktReceptors, CXCR4

Identifiers

PMID34136574
PMCPMC8179778
OpenAlexW3172109276

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.