Evidence map›Paper›PMID 21936900›Full record

ArticleMolecular pain2011

Targeting adenosine monophosphate-activated protein kinase (AMPK) in preclinical models reveals a potential mechanism for the treatment of neuropathic pain.

Ohannes K Melemedjian, Marina N Asiedu, Dipti V Tillu, Raul Sanoja, Jin Yan, Arianna Lark, Arkady Khoutorsky, Jessica Johnson, Katherine A Peebles, Talya Lepow and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

137 citing papers in PubMed, 220 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. GCN2 regulates paclitaxel-induced neuropathic pain.British journal of pharmacology · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Targeting Prefrontal Cortex Dysfunction in Pain.The Journal of pharmacology and experimental therapeutics · 2024
    Review
  13. Article
  14. Review
  15. Highly specific σProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Article
  18. Highly specific σbioRxiv : the preprint server for biology · 2023
    Article
  19. Article
  20. Article

77 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

13 authors at 2 institutions in 2 countries.

Ohannes K MelemedjianDepartment of Pharmacology, University of Arizona, N Campbell Ave, Tucson, 85724, USA.
Marina N Asiedu
Dipti V Tillu
Raul Sanoja
Jin Yan
Arianna Lark
Arkady Khoutorsky
Jessica Johnson
Katherine A Peebles
Talya Lepow
Nahum Sonenberg
Gregory Dussor
Theodore J Price
University of Arizona · USMcGill University · CA

Funding

Translation Control of Pain PlasticityR01NS065926 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI PRICE, THEODORE J. · 2010 to 2023
$5.7M
SHORT-TERM TRAINING STUDENTS IN HEALTH PROFESSIONAL SCHOT35HL007479 · NHLBI · UNIVERSITY OF ARIZONA · PI GEOFFREY C GURTNER, JAMES Kuang-Jan LIAO · 1985 to 2026
$4.4M
NHLBI NIH HHS T35HL007479NINDS NIH HHS R01 NS065926NINDS NIH HHS R01NS065926
6 · The paper itself

Abstract

Neuropathic pain is a debilitating clinical condition with few efficacious treatments, warranting development of novel therapeutics. We hypothesized that dysregulated translation regulation pathways may underlie neuropathic pain. Peripheral nerve injury induced reorganization of translation machinery in the peripheral nervous system of rats and mice, including enhanced mTOR and ERK activity, increased phosphorylation of mTOR and ERK downstream targets, augmented eIF4F complex formation and enhanced nascent protein synthesis. The AMP activated protein kinase (AMPK) activators, metformin and A769662, inhibited translation regulation signaling pathways, eIF4F complex formation, nascent protein synthesis in injured nerves and sodium channel-dependent excitability of sensory neurons resulting in a resolution of neuropathic allodynia. Therefore, injury-induced dysregulation of translation control underlies pathology leading to neuropathic pain and reveals AMPK as a novel therapeutic target for the potential treatment of neuropathic pain.

Indexed as

Molecular Targeted TherapyAction PotentialsAMP-Activated Protein Kinase KinasesAnimalsBlotting, WesternDisease Models, AnimalEnzyme ActivatorsEukaryotic Initiation Factor-4FHyperalgesiaMaleMiceMice, Inbred ICRNeuralgiaProtein BiosynthesisProtein KinasesRatsAMP-Activated Protein Kinase KinasesEnzyme ActivatorsEukaryotic Initiation Factor-4FProtein Kinases

Identifiers

PMID21936900
PMCPMC3186752
OpenAlexW2027889563

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.