Evidence map›Paper›PMID 33922596›Full record

ReviewInternational journal of molecular sciences2021

Targeting S1PRs as a Therapeutic Strategy for Inflammatory Bone Loss Diseases-Beyond Regulating S1P Signaling.

Hong Yu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. [Knockout of S1PR3 attenuates acute lung injury in mice by inhibiting the MAPK pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  10. [Research advances of the roles of sphingosine-1-phosphate in acute lung injury].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2022
    Review
  11. Article
  12. 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

1 author at 1 institution in 1 country.

Hong YuDepartment of Oral Health Sciences, College of Dental Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.ORCID 0000-0002-0930-6810
Medical University of South Carolina · US

Funding

Targeting sphingosine-1-phosphate receptor 2 as a novel therapeutic strategy for periodontitisR15DE027324 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI YU, HONG · 2018 to 2018
$437k
Role of sphingosine-1-phosphate receptor 2 in the pathogenesis of periodontitisR03DE025026 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI YU, HONG · 2015 to 2016
$224k
NIDCR NIH HHS R03 DE025026NIDCR NIH HHS R03DE025026NIDCR NIH HHS R15 DE027324NIDCR NIH HHS R15DE027324NIGMS NIH HHS R15DE027324
6 · The paper itself

Abstract

As G protein coupled receptors, sphingosine-1-phosphate receptors (S1PRs) have recently gained attention for their role in modulating inflammatory bone loss diseases. Notably, in murine studies inhibiting S1PR2 by its specific inhibitor, JTE013, alleviated osteoporosis induced by RANKL and attenuated periodontal alveolar bone loss induced by oral bacterial inflammation. Treatment with a multiple S1PRs modulator, FTY720, also suppressed ovariectomy-induced osteoporosis, collagen or adjuvant-induced arthritis, and apical periodontitis in mice. However, most previous studies and reviews have focused mainly on how S1PRs manipulate S1P signaling pathways, subsequently affecting various diseases. In this review, we summarize the underlying mechanisms associated with JTE013 and FTY720 in modulating inflammatory cytokine release, cell chemotaxis, and osteoclastogenesis, subsequently influencing inflammatory bone loss diseases. Studies from our group and from other labs indicate that S1PRs not only control S1P signaling, they also regulate signaling pathways induced by other stimuli, including bacteria, lipopolysaccharide (LPS), bile acid, receptor activator of nuclear factor κB ligand (RANKL), IL-6, and vitamin D. JTE013 and FTY720 alleviate inflammatory bone loss by decreasing the production of inflammatory cytokines and chemokines, reducing chemotaxis of inflammatory cells from blood circulation to bone and soft tissues, and suppressing RANKL-induced osteoclast formation.

Indexed as

AnimalsBone ResorptionHumansInflammationMolecular Targeted TherapySphingosine 1 Phosphate Receptor ModulatorsSphingosine-1-Phosphate ReceptorsSphingosine 1 Phosphate Receptor ModulatorsSphingosine-1-Phosphate Receptorsbone losschemotaxiscytokineFTY720JTE013osteoclastogenesissphingosine-1-phosphate receptors

Identifiers

PMID33922596
PMCPMC8122917
OpenAlexW3157651750

What OpenQuestion holds

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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.