Evidence map›Paper›PMID 30414411›Full record

ReviewThe American journal of pathology2019

Key Functions and Therapeutic Prospects of Nur77 in Inflammation Related Lung Diseases

Asoka Banno, Sowmya P Lakshmi, Aravind T Reddy, Seong C Kim, Raju C Reddy

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The synergistic effects of PMJournal of thoracic disease · 2025
    Article
  7. Article
  8. Article
  9. Nur77 Mediates Anaphylaxis by Regulating miR-21a.Current issues in molecular biology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Asoka BannoDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Sowmya P LakshmiDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania.
Aravind T ReddyDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania.
Seong C KimDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania.
Raju C ReddyDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania. Electronic address: reddyrc@upmc.edu.
University of Pittsburgh · US

Funding

PPAR-delta as a Novel Therapeutic Target in AsthmaR01AI125338 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REDDY, RAJU C · 2016 to 2020
$2.2M
Airway Epithelial Cell Farnesoid X Receptor in COPD PathophysiologyR01HL137842 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REDDY, RAJU C · 2017 to 2019
$1.2M
NHLBI NIH HHS R01 HL137842NIAID NIH HHS R01 AI125338
6 · The paper itself

Abstract

The transcription factor Nur77 belongs to the NR4A subfamily of nuclear hormone receptors. It features an atypical ligand-binding site that precludes canonical ligand binding, leading to the designation orphan nuclear receptor. However, recent studies show that small molecules can interact with the receptor and modulate its activity by inducing a conformational change in the Nur77 ligand-binding site. Nur77 expression and activation are rapidly induced by various physiological and pathologic stimuli. Once expressed, Nur77 initiates transcriptional activity and modulates expression of its target genes. Both in vitro and in vivo evidence shows that Nur77 dampens the immune response to proinflammatory stimuli, such as tumor necrosis factor-α, Toll-like receptor ligands, and oxidized lipids, primarily by suppressing NF-κB signaling. Although studies focusing on Nur77's role in lung pathophysiology are currently incomplete, available data support its involvement in the pathogenesis of lung diseases, including asthma, acute lung injury, and pulmonary fibrosis, and thus suggest a therapeutic potential for Nur77 activation in these diseases. This review addresses the mechanisms that control Nur77 as well as its known roles in inflammation-related lung diseases. Evidence regarding the therapeutic potential of Nur77-targeting molecules will also be presented. Although current knowledge is limited, additional research followed by clinical studies may firmly identify Nur77 as a pharmacologic target for inflammation-related lung diseases.

Indexed as

Signal TransductionTranscription, GeneticAnimalsHumansInflammationLungLung DiseasesNF-kappa BNuclear Receptor Subfamily 4, Group A, Member 1Toll-Like ReceptorsTumor Necrosis Factor-alphaNF-kappa BNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Toll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID30414411
PMCPMC6458520
OpenAlexW2900150319

What OpenQuestion holds

Textmetadata
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.