Evidence map›Paper›PMID 17548207›Full record

ReviewPharmacological research2007

Protein kinase C in pain: involvement of multiple isoforms.

Kandy T Velázquez, Husam Mohammad, Sarah M Sweitzer

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Pharmacological research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04542798 (Central Sensitization and Aberrant Nerve Sprouting Possible Explanations for RFA Failure of MBDR in CLBP of FJ Origin), which is not on this map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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.

NCT04542798 naunknown statusnot on this mapstarted 2020, after this paper: background citation

Central Sensitization and Aberrant Nerve Sprouting Possible Explanations for RFA Failure of MBDR in CLBP of FJ Origin: CRF Versus WCRF or PRF-DRG Randomized Clinical Trial

TypeinterventionalSponsorHospital General Universitario de ValenciaRan2020 to 2024Enrolled80ConditionsLow Back Pain, Recurrent, Neuropathic Pain, Facet Joint Pain, Central SensitisationArmsRadiofrequency COSMAN
3 · Its place in the literature

Who cites it

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. A proof-of-concept trial of protein kinase C iota inhibition with auranofin for the paclitaxel-induced acute pain syndrome.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2017
    Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
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  10. Review
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  13. Review
  14. Review
  15. Kinin BPharmaceutics · 2023
    Article
  16. Article
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  18. Article
  19. Article
  20. The redundancy and diversity between two novel PKC isotypes that regulate learning inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article

18 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 1 institution in 1 country.

Kandy T VelázquezDepartment of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Husam Mohammad
Sarah M Sweitzer
University of South Carolina · US

Funding

UofSC Postbaccalaureate Research Education ProgramR25GM066526 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ARMSTRONG, ALISSA RICHMOND, ELY, BERT · 2004 to 2024
$5.4M
University of South Carolina Initiative for Maximizing Student DevelopmentR25GM076277 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ELY, BERT · 2006 to 2015
$2.6M
Cellular and Molecular Regulation of Pediatric PainF32NS044729 · NINDS · STANFORD UNIVERSITY · PI SWEITZER, SARAH M · 2002 to 2003
$55k
NIGMS NIH HHS R25 GM066526NIGMS NIH HHS R25 GM076277NINDS NIH HHS F32 NS044729
6 · The paper itself

Abstract

Pain is the primary reason that people seek medical care. At present, chronic unremitting pain is the third greatest health problem after heart disease and cancer. Chronic pain is an economic burden in lost wages, lost productivity, medical expenses, legal fees and compensation. Chronic pain is defined as a pain of greater than 2 months duration. It can be of inflammatory or neuropathic origin that can arise following nerve injury or in the absence of any apparent injury. Chronic pain is characterized by an altered pain perception that includes allodynia (a response to a normally non-noxious stimuli) and hyperalgesia (an exaggerated response to a normally noxious stimuli). This type of pain is often insensitive to the traditional analgesics or surgical intervention. The study of the cellular and molecular mechanisms that contribute to chronic pain are of the up-most importance for the development of a new generation of analgesic agents. Protein kinase C isozymes are under investigation as potential therapeutics for the treatment of chronic pain conditions. The anatomical localization of protein kinase C isozymes in both peripheral and central nervous system sites that process pain have made them the topic of basic science research for close to two decades. This review will outline the research to date on the involvement of protein kinase C in pain and analgesia. In addition, this review will try to synthesize these works to begin to develop a comprehensive mechanistic understanding of how protein kinase C may function as a master regulator of the peripheral and central sensitization that underlies many chronic pain conditions.

Indexed as

Afferent PathwaysAnimalsBrainChronic DiseaseIsoenzymesNociceptorsPainPeripheral Nervous SystemProtein Kinase CSpinal CordSynapsesSynaptic TransmissionIsoenzymesProtein Kinase C

Identifiers

PMID17548207
PMCPMC2140050
OpenAlexW2072044677

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.