Evidence map›Paper›PMID 24988887›Full record

ArticleClinical and experimental immunology2014

Calreticulin promotes angiogenesis via activating nitric oxide signalling pathway in rheumatoid arthritis.

H Ding, C Hong, Y Wang, J Liu, N Zhang, C Shen, W Wei, F Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2014. 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
3.3field-weighted citation impact, top 9% 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, 28 citations in OpenAlex.

  1. Article
  2. ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. TNF-α/calreticulin dual signaling induced NLRP3 inflammasome activation associated with HuR nucleocytoplasmic shuttling in rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  8. Article
  9. Article
  10. Implications of Angiogenesis Involvement in Arthritis.International journal of molecular sciences · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Functional Analysis and Marker Development ofFrontiers in plant science · 2017
    Article
  17. 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

8 authors at 4 institutions in 1 country.

H DingDepartment of Immunology, School of Laboratory Medicine, Tianjin Medical University, Tianjin, China; The Second Hospital of Tangshan, Tangshan, China.
C Hong
Y Wang
J Liu
N Zhang
C Shen
W Wei
F Zheng
Tianjin Medical University · CNSecond Hospital of Tangshan · CNTianjin Medical University General Hospital · CNXi'an Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calreticulin (CRT) is a multi-functional endoplasmic reticulum protein implicated in the pathogenesis of rheumatoid arthritis (RA). The present study was undertaken to determine whether CRT was involved in angiogenesis via the activating nitric oxide (NO) signalling pathway. We explored the profile of CRT expression in RA (including serum, synovial fluid and synovial tissue). In order to investigate the role of CRT on angiogenesis, human umbilical vein endothelial cells (HUVECs) were isolated and cultured in this study for in-vitro experiments. Our results showed a significantly higher concentration of CRT in serum (5·4 ± 2·2 ng/ml) of RA patients compared to that of osteoarthritis (OA, 3·6 ± 0·9 ng/ml, P < 0·05) and healthy controls (HC, 3·7 ± 0·6 ng/ml, P < 0·05); and significantly higher CRT in synovial fluid (5·8 ± 1·2 ng/ml) of RA versus OA (3·7 ± 0·3 ng/ml, P < 0·05). High levels of CRT are expressed in synovial membrane localized predominantly to inflammatory cells and synovial perivascular areas in both the lining and sublining layers of RA synovial tissue (RAST). Increased nitric oxide (NO) production and phosphorylation level of endothelial nitric oxide synthase (eNOS) were measured in HUVECs following CRT stimulation, while the total eNOS expression was not significantly changed. Furthermore, CRT promoted the proliferation, migration and tube formation of HUVECs, which were significantly inhibited by a specific eNOS inhibitor. These findings suggested that CRT may be involved in angiogenesis events in RA through NO signalling pathways, which may provide a potential therapeutic target in the treatment of RA.

Indexed as

Signal TransductionAdultAgedArthritis, RheumatoidBlood SedimentationCalreticulinCell MovementCell ProliferationC-Reactive ProteinFemaleHumansHuman Umbilical Vein Endothelial CellsImmunohistochemistryMaleMiddle AgedNeovascularization, PathologicCalreticulinC-Reactive ProteinNitric OxideNitric Oxide Synthase Type IIIangiogenesiscalreticulinnitric oxiderheumatoid arthritis

Identifiers

PMID24988887
PMCPMC4233373
OpenAlexW1944587082

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.