Evidence map›Paper›PMID 30084208›Full record

ArticleCell proliferation2018

Cathepsin B regulates non-canonical NLRP3 inflammasome pathway by modulating activation of caspase-11 in Kupffer cells.

Nan Chen, Zhibing Ou, Wenfeng Zhang, Xiwen Zhu, Peizhi Li, Jianping Gong

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Embryo-Derived Cathepsin B Promotes Implantation and Decidualization by Activating Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  9. Review
  10. Inflammasome Molecular Insights in Autoimmune Diseases.Current issues in molecular biology · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Regulation of microglia polarization after cerebral ischemia.Frontiers in cellular neuroscience · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Nan ChenChongqing Key Laboratory of Hepatobiliary Surgery, Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID http://orcid.org/0000-0001-9825-2369
Zhibing OuChongqing Key Laboratory of Hepatobiliary Surgery, Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Wenfeng ZhangChongqing Key Laboratory of Hepatobiliary Surgery, Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xiwen ZhuDepartment of Anesthesia, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Peizhi LiChongqing Key Laboratory of Hepatobiliary Surgery, Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jianping GongChongqing Key Laboratory of Hepatobiliary Surgery, Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Dalian Medical University · CN

Funding

Basic Science and Frontier Technology Research Foundation of Chongqing science & technology commission cstc2015jcy jBX0070National Natural Science Foundation of China 31370753National Natural Science Foundation of China 81401622National Natural Science Foundation of China 81601715
6 · The paper itself

Abstract

objectivesThe non-canonical inflammasome pathway was described which engages caspase-11 to mediate pyroptosis and the subsequent release of IL-1α, IL-1β and IL-18 in TLR4-independent way. Cathepsin B is capable of activating caspase-11 under cell-free conditions which may regulate non-canonical NLRP3 inflammasome pathway. In this study, we aimed to further investigate cathepsin B as potential activators of proinflammatory caspases which may be released upon proinflammatory stimuli and regulate non-canonical NLRP3 inflammasome pathway by modulating the activity of caspase-11.

methodsPharmacological and gene-silencing approaches were used to evaluate the impact of cathepsin B on regulating non-canonical NLRP3 inflammasome pathway in wild-type and TLR4

resultsLPS stimulation caused cathepsin B activity and caspase-11 expression increase in TLR4

conclusionOur results suggest a critical role for cathepsin B as activators of proinflammatory caspases-11 and the regulatory effect in LPS-induced caspases-11-dependent necrosis.

Indexed as

AnimalsApoptosisCaspasesCaspases, InitiatorCathepsin BInflammasomesInterleukin-1betaKupffer CellsLeukocytes, MononuclearMacrophagesMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinCasp4 protein, mouseCaspasesCaspases, InitiatorCathepsin BInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouse

Identifiers

PMID30084208
PMCPMC6528937
OpenAlexW2887802841

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.