Evidence map›Paper›PMID 26113803›Full record

ArticleJournal of inflammation (London, England)2015

Nur77 deficiency leads to systemic inflammation in elderly mice.

Xiu-Ming Li, Xing-Xing Lu, Qian Xu, Jing-Ru Wang, Shen Zhang, Peng-Da Guo, Jian-Ming Li, Hua Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Vitamin A and retinoid signaling in the kidneys.Pharmacology & therapeutics · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Nur77 serves as a molecular brake of the metabolic switch during T cell activation to restrict autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. Article
  15. 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

8 authors at 1 institution in 1 country.

Xiu-Ming LiPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Xing-Xing LuPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Qian XuPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Jing-Ru WangPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Shen ZhangPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Peng-Da GuoPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Jian-Ming LiPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Hua WuPathology Center and Department of Pathology, Soochow University, Suzhou, 215123 China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNur77, an orphan member of the nuclear receptor superfamily, has been implicated in the regulation of inflammation. However, the in vivo function of Nur77 remains largely unexplored. In the current study, we investigated the role of Nur77 in inflammation and immunity in mice.

findingsWe found that elderly 8-month-old Nur77-deficient mice (Nur77(-/-)) developed systemic inflammation. Compared to wild-type (WT) mice (Nur77(+/+)), Nur77(-/-) mice showed splenomegaly, severe infiltration of inflammatory cells in several organs including liver, lung, spleen and kidney, increased hyperplasia of fibrous tissue in the lung and enlargement of kidney glomeruli. Additionally, Nur77(-/-) mice had increased production of pro-inflammatory cytokines and immunoglobulin, and elicited pro-inflammatory M1-like polarization in macrophages as revealed by increased expression of CXCL11 and INDO, and decreased expression of MRC1.

conclusionsThese in vivo observations provide evidence for a pivotal role for Nur77 in the regulation of systemic inflammation and emphasize the pathogenic significance of Nur77 in vivo.

Indexed as

Animal studyImmunityInflammationNur77

Identifiers

PMID26113803
PMCPMC4480882
OpenAlexW2145817460

What OpenQuestion holds

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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.