Evidence map›Paper›PMID 35107991›Full record

ReviewACS chemical neuroscience2022

Epigenetic Mechanisms of Neural Plasticity in Chronic Neuropathic Pain.

Krishna Ghosh, Hui-Lin Pan

Abstract readReview
In one paragraph

Review in ACS chemical neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.7field-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

47 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Histone Methyltransferase G9a in Primary Sensory Neurons Promotes Inflammatory Pain and Transcription ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Krishna GhoshCenter for Neuroscience and Pain Research, Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, United States.
Hui-Lin PanCenter for Neuroscience and Pain Research, Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, United States.ORCID 0000-0001-8444-3770
The University of Texas MD Anderson Cancer Center · US

Funding

Molecular Determinants of Synaptic Plasticity in Chronic PainR01NS101880 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Shao-Rui Chen, Hui-Lin Pan · 2017 to 2026
$4.1M
Mechanisms of Epigenetic Plasticity in Neuropathic PainR01NS132398 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Shao-Rui Chen, Hui-Lin Pan · 2023 to 2026
$1.8M
Neuronal Plasticity and Signaling in Neuropathic PainR01NS073935 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PAN, HUI-LIN · 2011 to 2015
$1.8M
NINDS NIH HHS R01 NS073935NINDS NIH HHS R01 NS101880NINDS NIH HHS R01 NS132398
6 · The paper itself

Abstract

Neuropathic pain is a challenging clinical problem and remains difficult to treat. Altered gene expression in peripheral sensory nerves and neurons due to nerve injury is well documented and contributes critically to the synaptic plasticity in the spinal cord and the initiation and maintenance of chronic pain. However, our understanding of the epigenetic mechanisms regulating the transcription of pro-nociceptive (e.g., NMDA receptors and α2δ-1) and antinociceptive (e.g., potassium channels and opioid and cannabinoid receptors) genes are still limited. In this review, we summarize recent studies determining the roles of histone modifications (including methylation, acetylation, and ubiquitination), DNA methylation, and noncoding RNAs in neuropathic pain development. We review the epigenetic writer, reader, and eraser proteins that participate in the transcriptional control of the expression of key ion channels and neurotransmitter receptors in the dorsal root ganglion after traumatic nerve injury, which is commonly used as a preclinical model of neuropathic pain. A better understanding of epigenetic reprogramming involved in the transition from acute to chronic pain could lead to the development of new treatments for neuropathic pain.

Indexed as

NeuralgiaEpigenesis, GeneticGanglia, SpinalHumansNeuronal PlasticitySpinal CordChromatinDRG neuronepigeneticsG9aneuron-restrictive silencer factorNMDA receptornociceptorpotassium channelspinal cord

Identifiers

PMID35107991
PMCPMC13294747
OpenAlexW4210524333

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.