Evidence map›Paper›PMID 29771006›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2018

The Antifibrotic Effect of A

Harry Karmouty-Quintana, Jose G Molina, Kemly Philip, Chiara Bellocchi, Brent Gudenkauf, Minghua Wu, Ning-Yuan Chen, Scott D Collum, Junsuk Ko, Sandeep K Agarwal and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis.International journal of molecular sciences · 2021
    Review
  11. Adenosine Signaling in Autoimmune Disorders.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. Review
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

14 authors at 4 institutions in 2 countries.

Harry Karmouty-QuintanaMcGovern Medical School, Houston, Texas.
Jose G MolinaMcGovern Medical School, Houston, Texas.
Kemly PhilipMcGovern Medical School, Houston, Texas.
Chiara BellocchiMcGovern Medical School, Houston, Texas, Referral Center for Systemic Autoimmune Diseases, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy.
Brent GudenkaufMcGovern Medical School, Houston, Texas, Texas Tech University Health Sciences Center, Lubbock.
Minghua WuMcGovern Medical School, Houston, Texas.
Ning-Yuan ChenMcGovern Medical School, Houston, Texas.
Scott D CollumMcGovern Medical School, Houston, Texas.
Junsuk KoMcGovern Medical School, Houston, Texas.
Sandeep K AgarwalBaylor College of Medicine, Houston, Texas.
Shervin AssassiMcGovern Medical School, Houston, Texas.
Hongyan ZhongGilead Sciences, Inc., Foster City, California.
Michael R BlackburnMcGovern Medical School, Houston, Texas.
Tingting WengMcGovern Medical School, Houston, Texas.
Gilead Sciences (United States) · USFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITBaylor College of Medicine · USTexas Tech University · US

Funding

CFlm25 mediated alternative polyadenylation regulates fibrosis in systemic sclerosisR01AR073284 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ASSASSI, SHERVIN, MILLS, TINGTING WENG · 2019 to 2023
$1.7M
American Heart Association-American Stroke Association 12POST11810007NIAMS NIH HHS R01 AR073284
6 · The paper itself

Abstract

objectiveSystemic sclerosis (SSc; scleroderma) is a chronic disease that affects the skin and various internal organs. Dermal fibrosis is a major component of this disease. The mechanisms that promote dermal fibrosis remain elusive. Elevations in tissue adenosine levels and the subsequent engagement of the profibrotic A

methodsWe assessed the involvement of ADORA2B in the regulation of dermal fibrosis using a well-established mouse model of dermal fibrosis. Using an orally active ADORA2B antagonist, we demonstrated how inhibition of ADORA2B results in reduced dermal fibrosis in 2 distinct experimental models. Finally, using human dermal fibroblasts, we characterized the expression of adenosine receptors.

resultsWe demonstrated that levels of ADORA2B were significantly elevated in dermal fibrosis and that the therapeutic blockade of this receptor in vivo using an ADORA2B antagonist could reduce the production of profibrotic mediators in the skin and attenuate dermal fibrosis. Antagonism of ADORA2B resulted in reduced numbers of arginase-expressing macrophages and myofibroblasts and in reduced levels of the extracellular matrix proteins fibronectin, collagen, and hyaluronan.

conclusionThese findings identify ADORA2B as a potential profibrotic regulator in dermal fibrosis and suggest that ADORA2B antagonism may be a useful approach for the treatment of SSc.

Indexed as

AnimalsBleomycinDisease Models, AnimalFibroblastsFibrosisHumansMaleMiceMice, Inbred C57BLPurinergic P1 Receptor AntagonistsScleroderma, SystemicSkinSkin DiseasesBleomycinPurinergic P1 Receptor Antagonists

Identifiers

PMID29771006
PMCPMC10077881
OpenAlexW2803755451

What OpenQuestion holds

Textmetadata
LicenceTDM
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.