Evidence map›Paper›PMID 26960759›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2016

Egr-1 deficiency protects from renal inflammation and fibrosis.

Li-Chun Ho, Junne-Ming Sung, Yi-Ting Shen, Huei-Fen Jheng, Shun-Hua Chen, Pei-Jane Tsai, Yau-Sheng Tsai

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.9field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Lipid Deposition Profiles Influence Foreign Body Responses.Advanced materials (Deerfield Beach, Fla.) · 2023
    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

7 authors at 3 institutions in 1 country.

Li-Chun HoInstitute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.
Junne-Ming SungDepartment of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, Republic of China.
Yi-Ting ShenDepartment of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, Republic of China.
Huei-Fen JhengInstitute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.
Shun-Hua ChenDepartment of Microbiology and Immunology, National Cheng Kung University, Tainan, Taiwan, Republic of China.
Pei-Jane TsaiDepartment of Medical Laboratory Science and Biotechnology, National Cheng Kung University, Tainan, Taiwan, Republic of China.
Yau-Sheng TsaiInstitute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China. yaustsai@mail.ncku.edu.tw.
National Cheng Kung University · TWNational Cheng Kung University Hospital · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledNF-κB and TGFβ play critical roles in renal inflammation and fibrosis, and their regulation in the kidney is thus of great interest. Early growth response-1 (Egr-1), a transcription factor belonging to the immediate early gene family, has been found to regulate inflammation and fibrosis in non-kidney tissues, but its role in renal failure has not been clear. In this study, wild-type and Egr1 (-/-) mice were fed with an adenine-enriched diet to induce tubulointerstitial nephritis (TIN), and primary tubular epithelial cells (PTECs) were treated with pro-inflammatory and pro-fibrotic cytokines. Kidney tissues from patients with or without renal failure were stained for Egr-1. Our results showed that Egr-1 expression was upregulated in the kidney with TIN, and the tubular epithelial cell is the primary site for Egr-1 upregulation and nuclear translocation. Egr1 (-/-) mice were protected from renal failure, reflected by low levels of serum urea and creatinine. The protective effect was related to an attenuation of tubular injury, immune cell infiltration, NF-κB activity, and cytokine/chemokine expressions in the kidney. Renal fibrotic area and TGFβ signaling were also reduced in Egr1 (-/-) mice. In vitro study showed that Egr-1 deficiency attenuated the ordinary responses of PTECs to TNFα and TGFβ. Importantly, Egr-1 is of clinical significance since the activity of Egr-1 in renal tubular cells was upregulated in renal failure patients. Our study highlights the integrative role of Egr-1 in renal inflammation and fibrosis. Thus, Egr-1 may serve as a therapeutic target for human kidney diseases. KEY MESSAGES: Renal failure activates Egr-1 in human and mouse tubular cells. Egr-1 deficiency attenuates NF-κB and TGFβ-mediated renal inflammation/fibrosis. Egr1 (-/-) PTECs respond weakly to pro-inflammatory or pro-fibrotic stimulation.

Indexed as

AnimalsCells, CulturedEarly Growth Response Protein 1FibrosisGene Knockout TechniquesHumansKidneyMice, Inbred C57BLMice, KnockoutNephritis, InterstitialNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinTransforming Growth Factor betaEarly Growth Response Protein 1Egr1 protein, mouseNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseTransforming Growth Factor betaEarly growth response-1NLRP3 inflammasomeRenal failureRenal fibrosisRenal inflammation

Identifiers

PMID26960759
OpenAlexW2294057964

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.