Evidence map›Paper›PMID 35832027›Full record

ArticleAging2022

NOX4 promotes Kupffer cell inflammatory response via ROS-NLRP3 to aggravate liver inflammatory injury in acute liver injury.

Liping Zhai, Hongyan Pei, Yi Yang, Yu Zhu, Shuiliang Ruan

Abstract read
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Stem cell-based therapeutic strategies for liver aging.Liver research (Beijing, China) · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
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.

Liping ZhaiThe Second Affiliated Hospital of Jiaxing University, Zhejiang 314001, China.
Hongyan PeiJilin Agricultural University, Changchun 130000, China.
Yi YangThe Second Affiliated Hospital of Jiaxing University, Zhejiang 314001, China.
Yu ZhuThe Second Affiliated Hospital of Jiaxing University, Zhejiang 314001, China.
Shuiliang RuanThe Second Affiliated Hospital of Jiaxing University, Zhejiang 314001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThis work aimed to investigate the mechanism of NOX4 in promoting Kupffer cells (KCs) activation and tissue inflammatory response in acute liver injury.

methodsInitially, the mouse KCs were cultured

resultsLPS induced KCs inflammatory response. NOX4 overexpression decreased the mouse viability and increased the apoptosis rate. The levels of inflammatory factors were up-regulated in the culture medium. In addition, ROS were activated, and the positive cell number increased. Moreover, NOX4 promoted NLRP3 activation and significantly increased the expression of NLRP3 and ASC. Pretreatment with NOX4 inhibitor or NAC antagonized the effects of NOX4 and suppressed the KCs inflammatory response. In the mouse model, NOX4 knockdown significantly suppressed the activation and inflammatory response of microglial cells in tissues, reducing the NLRP3 expression in tissues.

conclusionNOX4 activates the NLRP3 inflammasome via ROS to promote inflammatory response in KCs and the release of inflammatory factors, suppressing NOX4 can improve ALI in mice, and NOX4 is promising as a new target for ALI treatment.

Indexed as

InflammasomesKupffer CellsAnimalsCaspase 1Disease Models, AnimalLipopolysaccharidesLiverMiceNADPH Oxidase 4NigericinNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesCaspase 1InflammasomesLipopolysaccharidesNADPH Oxidase 4NigericinNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseNox4 protein, mouseReactive Oxygen Speciesacute liver injuryinflammatory responseKupfferNOX4ROS

Identifiers

PMID35832027
PMCPMC9512511

What OpenQuestion holds

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Registered trials

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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.