Evidence map›Paper›PMID 26521775›Full record

ReviewCurrent drug targets2016

Adenosine Monophosphate-activated Protein Kinase (AMPK) Activators For the Prevention, Treatment and Potential Reversal of Pathological Pain.

Theodore J Price, Vaskar Das, Gregory Dussor

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Endocannabinoid biosynthetic enzymes regulate pain response via LKB1-AMPK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Chemotherapy-Induced Peripheral Neuropathy.Handbook of experimental pharmacology · 2023
    Article
  14. Article
  15. Review
  16. Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Review
  17. Article
  18. Metformin: A Potential Therapeutic Tool for Rheumatologists.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Theodore J PriceSchool of Behavioral and Brain Sciences, University of Texas at Dallas, JO 4.212 800 W Campbell Rd, Richardson TX 75080, USA. Theodore.price@utdallas.edu.
Vaskar Das
Gregory Dussor
Institut des Sciences Cognitives Marc Jeannerod · FR

Funding

Translation Control of Pain PlasticityR01NS065926 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI PRICE, THEODORE J. · 2010 to 2023
$5.7M
AMPK ACTIVATORS FOR THE TREATMENT OF POST-SURGICAL PAINR01GM102575 · NIGMS · UNIVERSITY OF TEXAS DALLAS · PI DUSSOR, GREGORY O, PRICE, THEODORE J. · 2013 to 2016
$1.1M
NIGMS NIH HHS R01 GM102575NINDS NIH HHS R01 NS065926
6 · The paper itself

Abstract

Pathological pain is an enormous medical problem that places a significant burden on patients and can result from an injury that has long since healed or be due to an unidentifiable cause. Although treatments exist, they often either lack efficacy or have intolerable side effects. More importantly, they do not reverse the changes in the nervous system mediating pathological pain, and thus symptoms often return when therapies are discontinued. Consequently, novel therapies are urgently needed that have both improved efficacy and disease-modifying properties. Here we highlight an emerging target for novel pain therapies, adenosine monophosphate-activated protein kinase (AMPK). AMPK is capable of regulating a variety of cellular processes including protein translation, activity of other kinases, and mitochondrial metabolism, many of which are thought to contribute to pathological pain. Consistent with these properties, preclinical studies show positive, and in some cases disease-modifying effects of either pharmacological activation or genetic regulation of AMPK in models of nerve injury, chemotherapy-induced peripheral neuropathy (CIPN), postsurgical pain, inflammatory pain, and diabetic neuropathy. Given the AMPK-activating ability of metformin, a widely prescribed and well-tolerated drug, these preclinical studies provide a strong rationale for both retrospective and prospective human pain trials with this drug. They also argue for the development of novel AMPK activators, whether orthosteric, allosteric, or modulators of events upstream of the kinase. Together, this review will present the case for AMPK as a novel therapeutic target for pain and will discuss future challenges in the path toward development of AMPK-based pain therapeutics.

Indexed as

AMP-Activated Protein KinasesAnalgesicsAnimalsHumansMitochondriaPainSignal TransductionAMP-Activated Protein KinasesAnalgesics

Identifiers

PMID26521775
PMCPMC4852160
OpenAlexW2137094819

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.