Evidence map›Paper›PMID 28215032›Full record

ArticleImmunologic research2017

NLRP3 inflammasome activation regulated by NF-κB and DAPK contributed to paraquat-induced acute kidney injury.

Zhenning Liu, Xiaokai Wang, Yu Wang, Min Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Immunologic research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Loss of sphingosine kinase 2 protects against cisplatin-induced kidney injury.American journal of physiology. Renal physiology · 2022
    Article
  10. Article
  11. Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022
    Review
  12. Article
  13. Article
  14. Review
  15. S1P/S1PAntioxidants (Basel, Switzerland) · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Zhenning LiuDepartment of Emergency Medicine, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.
Xiaokai WangDepartment of Pathology, The General Hospital of Shenyang Military, No. 83, Wenhua Road, Shenhe District, Shenyang, 110016, China.
Yu WangDepartment of Emergency Medicine, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.
Min ZhaoDepartment of Emergency Medicine, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China. wfzd999@126.com.
China Medical University · CNGeneral Hospital of Shenyang Military Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paraquat can result in dysfunction of multiple organs after ingestion in human. However, the mechanisms of nucleotide-binding domain and leucine-rich repeat containing protein 3 (NLRP3) inflammasome activation in acute kidney injury have not been clearly demonstrated. The aim of this study was to determine the effect of NLRP3 inflammasome activation and its regulation by nuclear factor-kappa B (NF-κB) and death-associated protein kinase (DAPK). Male Wistar rats were treated with intraperitoneal injection of paraquat at 20 mg/kg, and NF-κB inhibitor BAY 11-7082 was pretreated at 10 mg/kg 1 h before paraquat exposure. Additionally, rat renal tubular epithelial cells (NRK-52E) were transfected with small interfering RNA (siRNA) against DAPK to evaluate its role in NLRP3 inflammasome activation. DAPK and NLRP3 inflammasome were evaluated by immunohistochemistry staining or Western blot; the pro-inflammatory cytokines including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-18 (IL-18) were measured via ELISA. The results showed that NF-κB, DAPK, and NLRP3 inflammasome were activated in paraquat (PQ)-treated rat kidney; the secretion of pro-inflammatory cytokines was significantly increased. These toxic effects were attenuated by NF-κB inhibitor. Besides, the activation of NLRP3 inflammasome and secretion of IL-1β and IL-18 in paraquat-treated rat renal tubular epithelial cells were inhibited by siRNA against DAPK. In conclusion, NLRP3 inflammasome activation regulated by NF-κB and DAPK played an important role in paraquat-induced acute kidney injury.

Indexed as

Acute Kidney InjuryAnimalsCells, CulturedCytokinesDeath-Associated Protein KinasesEpithelial CellsHumansInflammasomesInflammation MediatorsKidney TubulesMaleNF-kappa BNitrilesNLR Family, Pyrin Domain-Containing 3 ProteinParaquatRats3-(4-methylphenylsulfonyl)-2-propenenitrileCytokinesDeath-Associated Protein KinasesInflammasomesInflammation MediatorsNF-kappa BNitrilesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratParaquatRNA, Small InterferingSulfonesAcute kindey injuryDAPKNF-κBNLRP3 inflammasomeParaquat

Identifiers

PMID28215032
OpenAlexW2587872582

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.