Evidence map›Paper›PMID 23592612›Full record

ReviewPharmacological reviews2013

Adenosine kinase: exploitation for therapeutic gain.

Detlev Boison

Open access · bronzeAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 2 pooled it
17.2field-weighted citation impact, top 1% 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

189 citing papers in PubMed, 2 syntheses or guidelines pooled it, 313 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Modern Analytical Techniques in Epilepsy Research.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Adenosine in the Brain: Recent Progress on Detection, Function, and Translation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  14. Review
  15. Neurocognitive and neurobiological effects of low dose organophosphate exposure.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

129 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

1 author at 1 institution in 1 country.

Detlev BoisonLegacy Research Institute, 1225 NE 16th Ave, Portland, OR 97202, USA. dboison@downeurobiology.org
Legacy Health · US

Funding

The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
Adenosine and schizophrenia: mechanisms and therapiesR01MH083973 · NIMH · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2009 to 2015
$2.5M
Astrocyte dysfunction in epileptogenesis: the role of adenosineR01NS061844 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2009 to 2013
$1.5M
NIMH NIH HHS MH083973NIMH NIH HHS R01 MH083973NINDS NIH HHS NS061844NINDS NIH HHS NS065957NINDS NIH HHS R01 NS061844NINDS NIH HHS R01 NS065957
6 · The paper itself

Abstract

Adenosine kinase (ADK; EC 2.7.1.20) is an evolutionarily conserved phosphotransferase that converts the purine ribonucleoside adenosine into 5'-adenosine-monophosphate. This enzymatic reaction plays a fundamental role in determining the tone of adenosine, which fulfills essential functions as a homeostatic and metabolic regulator in all living systems. Adenosine not only activates specific signaling pathways by activation of four types of adenosine receptors but it is also a primordial metabolite and regulator of biochemical enzyme reactions that couple to bioenergetic and epigenetic functions. By regulating adenosine, ADK can thus be identified as an upstream regulator of complex homeostatic and metabolic networks. Not surprisingly, ADK dysfunction is involved in several pathologies, including diabetes, epilepsy, and cancer. Consequently, ADK emerges as a rational therapeutic target, and adenosine-regulating drugs have been tested extensively. In recent attempts to improve specificity of treatment, localized therapies have been developed to augment adenosine signaling at sites of injury or pathology; those approaches include transplantation of stem cells with deletions of ADK or the use of gene therapy vectors to downregulate ADK expression. More recently, the first human mutations in ADK have been described, and novel findings suggest an unexpected role of ADK in a wider range of pathologies. ADK-regulating strategies thus represent innovative therapeutic opportunities to reconstruct network homeostasis in a multitude of conditions. This review will provide a comprehensive overview of the genetics, biochemistry, and pharmacology of ADK and will then focus on pathologies and therapeutic interventions. Challenges to translate ADK-based therapies into clinical use will be discussed critically.

Indexed as

Molecular Targeted TherapyAdenosine KinaseAnimalsDrug DesignEnergy MetabolismEnzyme InhibitorsEpigenesis, GeneticHumansSignal TransductionAdenosine KinaseEnzyme Inhibitors

Identifiers

PMID23592612
PMCPMC3698936
OpenAlexW2146632088

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.