Evidence map›Paper›PMID 23340998›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2013

Adenosine signaling during acute and chronic disease states.

Harry Karmouty-Quintana, Yang Xia, Michael R Blackburn

Abstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Blockage of the adenosine APurinergic signalling · 2024
    Article
  11. Article
  12. Article
  13. Targeting Cancer Metabolism to Improve Outcomes with Immune Checkpoint Inhibitors.Journal of immunotherapy and precision oncology · 2023
    Review
  14. Review
  15. Hyaluronan in the pathogenesis of acute and post-acute COVID-19 infection.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

20 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Harry Karmouty-QuintanaDepartment of Biochemistry and Molecular Biology, The University of Texas Medical School at Houston, 6431 Fannin Blvd, Suite 6.200, Houston, TX 77030, USA.
Yang Xia
Michael R Blackburn
The University of Texas at Austin · USThe University of Texas Health Science Center at Houston · US

Funding

Adenosine Signaling and Lung FibrosisR01HL070952 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BLACKBURN, MICHAEL R · 2002 to 2019
$5.7M
Adenosine Signaling, Priapism and Sickle Cell DiseaseR01DK083559 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI XIA, YANG · 2009 to 2012
$1.3M
NHLBI NIH HHS HL070952NHLBI NIH HHS R01 HL070952NIDDK NIH HHS DK083559NIDDK NIH HHS R01 DK083559
6 · The paper itself

Abstract

Adenosine is a signaling nucleoside that is produced following tissue injury, particularly injury involving ischemia and hypoxia. The production of extracellular adenosine and its subsequent signaling through adenosine receptors plays an important role in orchestrating injury responses in multiple organs. There are four adenosine receptors that are widely distributed on immune, epithelial, endothelial, neuronal,and stromal cells throughout the body. Interestingly, these receptors are subject to altered regulation following injury. Studies in mouse models and human cells and tissues have identified that the production of adenosine and its subsequent signaling through its receptors plays largely beneficial roles in acute disease states, with the exception of brain injury. In contrast, if elevated adenosine levels are sustained beyond the acute injury phase, adenosine responses can become detrimental by activating pathways that promote tissue injury and fibrosis. Understanding when during the course of disease adenosine signaling is beneficial as opposed to detrimental and defining the mechanisms involved will be critical for the advancement of adenosine-based therapies for acute and chronic diseases. The purpose of this review is to discuss key observations that define the beneficial and detrimental aspects of adenosine signaling during acute and chronic disease states with an emphasis on cellular processes, such as inflammatory cell regulation, vascular barrier function, and tissue fibrosis.

Indexed as

Acute DiseaseAdenosineAnimalsChronic DiseaseHumansSignal TransductionAdenosine

Identifiers

PMID23340998
PMCPMC3606047
OpenAlexW2130202913

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.