Evidence map›Paper›PMID 37559537›Full record

ReviewCurrent neuropharmacology2024

Peripheral Neuroinflammation and Pain: How Acute Pain Becomes Chronic.

Mark A Schumacher

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current neuropharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 3 pooled it
6.5field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 3 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  7. Minor cannabinoids CBD, CBG, CBN, and CBC differentially modulate sensory neuron activation.The Journal of pharmacology and experimental therapeutics · 2026
    Article
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  17. Developing the FIGO-IPPS "R U MOVVING SOMe" classification system for female chronic pelvic pain.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025
    Article
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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.

Mark A SchumacherDepartment of Anesthesia and Perioperative Care and the UCSF Pain and Addiction Research Center, University of California, San Francisco, California, 94143 USA.
University of California, San Francisco · US

Funding

Chronic Chemotherapy Peripheral Neuropathy: Role of Neuroplasticity and StressR01CA250017 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEVINE, JON DAVID · 2019 to 2023
$3.3M
NIH HHS NIH R01CA250017
6 · The paper itself

Abstract

The number of individuals suffering from severe chronic pain and its social and financial impact is staggering. Without significant advances in our understanding of how acute pain becomes chronic, effective treatments will remain out of reach. This mini review will briefly summarize how critical signaling pathways initiated during the early phases of peripheral nervous system inflammation/ neuroinflammation establish long-term modifications of sensory neuronal function. Together with the recruitment of non-neuronal cellular elements, nociceptive transduction is transformed into a pathophysiologic state sustaining chronic peripheral sensitization and pain. Inflammatory mediators, such as nerve growth factor (NGF), can lower activation thresholds of sensory neurons through posttranslational modification of the pain-transducing ion channels transient-receptor potential TRPV1 and TRPA1. Performing a dual role, NGF also drives increased expression of TRPV1 in sensory neurons through the recruitment of transcription factor Sp4. More broadly, Sp4 appears to modulate a nociceptive transcriptome including TRPA1 and other genes encoding components of pain transduction. Together, these findings suggest a model where acute pain evoked by peripheral injury-induced inflammation becomes persistent through repeated cycles of TRP channel modification, Sp4-dependent overexpression of TRP channels and ongoing production of inflammatory mediators.

Indexed as

Acute PainTransient Receptor Potential ChannelsHumansInflammationInflammation MediatorsNerve Growth FactorNeuroinflammatory DiseasesTRPV Cation ChannelsInflammation MediatorsNerve Growth FactorTransient Receptor Potential ChannelsTRPV Cation ChannelsChronic paininflammationNGFsensory neurontranscription factorTRPA1TRPV1.

Identifiers

PMID37559537
PMCPMC10716877
OpenAlexW4385716526

What Socratic 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 Socratic graph.