Evidence map›Paper›PMID 32403409›Full record

ReviewCells2020

Function and Mechanisms of Truncated BDNF Receptor TrkB.T1 in Neuropathic Pain.

Tuoxin Cao, Jessica J Matyas, Cynthia L Renn, Alan I Faden, Susan G Dorsey, Junfang Wu

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Review
  3. Disruption of BDNF signalling in neuropathologies.Biochemical Society transactions · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  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

6 authors at 1 institution in 1 country.

Tuoxin CaoDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Jessica J MatyasDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Cynthia L RennDepartment of Pain and Translational Symptom Science, University of Maryland School of Nursing, Baltimore, MD 21201, USA.ORCID 0000-0001-6764-9347
Alan I FadenDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Susan G DorseyDepartment of Pain and Translational Symptom Science, University of Maryland School of Nursing, Baltimore, MD 21201, USA.ORCID 0000-0001-7648-1312
Junfang WuDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD 21201, USA.ORCID 0000-0003-3338-7291
University of Maryland, Baltimore · US

Funding

Spinal Mechanisms Underlying SCI-Induced Pain: Implications for Targeted TherapyR01NR013601 · NINR · UNIVERSITY OF MARYLAND BALTIMORE · PI DORSEY, SUSAN G, FADEN, ALAN IRA · 2012 to 2021
$6.0M
The new roles of the autophagy-lysosomal pathway in spinal cord injury-mediated dementiaR01NS094527 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI MARTA M LIPINSKI, Junfang Wu · 2016 to 2026
$3.5M
Dementia Following Spinal Cord Injury: Mechanism and Therapeutic TargetingRF1NS110637 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI JAY, STEVEN MICHAEL, WU, JUNFANG · 2019 to 2019
$2.8M
Mechanism of Inflammatory Related Brain Dysfunction after Spinal Cord InjuryR01NS110635 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI FADEN, ALAN IRA, WU, JUNFANG · 2019 to 2023
$2.2M
NINDS NIH HHS R01 NS094527NINDS NIH HHS R01 NS110635NINDS NIH HHS RF1 NS110637NINR NIH HHS R01 NR013601
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF), a major focus for regenerative therapeutics, has been lauded for its pro-survival characteristics and involvement in both development and recovery of function within the central nervous system (CNS). However, studies of tyrosine receptor kinase B (TrkB), a major receptor for BDNF, indicate that certain effects of the TrkB receptor in response to disease or injury may be maladaptive. More specifically, imbalance among TrkB receptor isoforms appears to contribute to aberrant signaling and hyperpathic pain. A truncated isoform of the receptor, TrkB.T1, lacks the intracellular kinase domain of the full length receptor and is up-regulated in multiple CNS injury models. Such up-regulation is associated with hyperpathic pain, and TrkB.T1 inhibition reduces neuropathic pain in various experimental paradigms. Deletion of TrkB.T1 also limits astrocyte changes in vitro, including proliferation, migration, and activation. Mechanistically, TrkB.T1 is believed to act through release of intracellular calcium in astrocytes, as well as through interactions with neurotrophins, leading to cell cycle activation. Together, these studies support a potential role for astrocytic TrkB.T1 in hyperpathic pain and suggest that targeted strategies directed at this receptor may have therapeutic potential.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorEmbryonic DevelopmentHumansMutant ProteinsNeuralgiaReceptor, trkBSignal TransductionBrain-Derived Neurotrophic FactorMutant ProteinsReceptor, trkBastrocytesbrain-derived neurotrophic factor (BDNF)neuropathic painspinal cord injuryTrkB.T1tyrosine receptor kinase B (TrkB)

Identifiers

PMID32403409
PMCPMC7290366
OpenAlexW3023624746

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.