Evidence map›Paper›PMID 29193850›Full record

ArticleInternational forum of allergy & rhinology2018

Olfactory loss in chronic rhinosinusitis is associated with neuronal activation of c-Jun N-terminal kinase.

Andrew J Victores, Mengfei Chen, Amy Smith, Andrew P Lane

Abstract read
In one paragraph

Article in International forum of allergy & rhinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Olfactory Loss in Rhinosinusitis: Mechanisms of Loss and Recovery.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Immunological Aspects of Chronic Rhinosinusitis.Diagnostics (Basel, Switzerland) · 2022
    Review
  14. International consensus statement on allergy and rhinology: Olfaction.International forum of allergy & rhinology · 2022
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

4 authors.

Andrew J VictoresDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.ORCID 0000-0001-8879-2732
Mengfei ChenDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Amy SmithDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Andrew P LaneDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.

Funding

Chronic rhinosinusitis-associated olfactory lossR01DC009026 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI LANE, ANDREW P · 2008 to 2015
$2.9M
NIDCD NIH HHS R01 DC009026
6 · The paper itself

Abstract

backgroundOlfactory inflammation in chronic rhinosinusitis (CRS) is associated with cytokines that may result in the death of olfactory sensory neurons. The principal signaling molecules involved in the apoptotic pathway are c-Jun N-terminal kinases (JNK). Although the JNK pathway has emerged as a key player in programmed cell death in neuroinflammation, its specific role in CRS-associated olfactory loss has not been thoroughly investigated.

methodsJNK activation was studied in human tissue samples from 9 control and 11 CRS patients by immunohistochemical staining for phosphorylated c-Jun. A mouse model of inducible olfactory cytokine expression was used to experimentally control inflammation and assess JNK activation over time.

resultsIn patients with CRS, activation of c-Jun is significantly increased relative to non-CRS control subjects, and there is an associated loss of sensory neurons. In the olfactory inflammation mouse model, prolonged induction of inflammation results in elevation of c-Jun expression and neuronal apoptosis.

conclusionActivation of neuronal JNK is a feature of chronic olfactory inflammation that is associated with neuronal apoptosis. Given that inhibition of JNK activity is neuroprotective in other settings, antagonism of this pathway may have therapeutic potential in the management of inflammatory olfactory loss or other disorders linked to olfactory neuronal apoptosis.

Indexed as

AdultAgedAnimalsChronic DiseaseFemaleHumansJNK Mitogen-Activated Protein KinasesMaleMice, KnockoutMiddle AgedOlfaction DisordersOlfactory Receptor NeuronsReceptors, Tumor Necrosis Factor, Type IRespiratory Tract DiseasesJNK Mitogen-Activated Protein KinasesReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, mousechronic rhinosinusitisinflammationJNKolfaction, olfactory disordersolfactory sensory neurons

Identifiers

PMID29193850
PMCPMC5842118

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.