Evidence map›Paper›PMID 28423922›Full record

ReviewExperimental biology and medicine (Maywood, N.J.)2017

Activation of GPR15 and its involvement in the biological effects of smoking.

Sulev Kõks, Gea Kõks

Abstract readReview
In one paragraph

Review in Experimental biology and medicine (Maywood, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Article
  2. Review
  3. Cardiovascular Disease and Psoriasis.Dermatology and therapy · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The Role of GPR15 Function in Blood and Vasculature.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. 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

2 authors.

Sulev Kõks1 Department of Pathophysiology, University of Tartu, Tartu 50411, Estonia.
Gea Kõks1 Department of Pathophysiology, University of Tartu, Tartu 50411, Estonia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smoking is one of the most significant modifiable environmental risk factors for many diseases. Smoking causes excessive mortality worldwide. Despite decades of long research, there has not been a clear understanding regarding the molecular mechanism that makes smoking harmful to health. Some recent studies have found that smoking influences most significantly the expression and methylation of GPR15. GPR15 is an orphan receptor that is involved in the regulation of the innate immunity and the T-cell trafficking in the intestinal epithelium. Further studies have confirmed that GPR15 is very strongly involved in smoking and smoking-induced molecular changes. Therefore, the altered expression and epigenetic regulation of GPR15 could have a significant role in the health impact of smoking. Impact statement The review describes an orphan receptor GPR15 that has recently been found to be influenced by smoking. This makes GPR15 very sensitive and adequate biomarker for smoking and smoking studies. Also, activation of GPR15 by smoking could help to explain its effects on health.

Indexed as

Epigenesis, GeneticHumansMethylationProtein Processing, Post-TranslationalReceptors, G-Protein-CoupledReceptors, PeptideSmokingGPR15 protein, humanReceptors, G-Protein-CoupledReceptors, PeptideepigeneticsgenomicsGPR15immunologyTobacco smokingtranscriptome

Identifiers

PMID28423922
PMCPMC5478000

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.