Evidence map›Paper›PMID 33375031›Full record

ArticleInternational journal of molecular sciences2020

ANP and BNP Exert Anti-Inflammatory Action via NPR-1/cGMP Axis by Interfering with Canonical, Non-Canonical, and Alternative Routes of Inflammasome Activation in Human THP1 Cells.

Letizia Mezzasoma, Vincenzo Nicola Talesa, Rita Romani, Ilaria Bellezza

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. NLRP3 inflammasome: a key player in neonatal brain injury.Clinical and experimental pediatrics · 2025
    Article
  7. Article
  8. Review
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  10. Article
  11. Review
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  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Therapeutic implications of inflammasome in inflammatory bowel disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Review
  19. Article
  20. The Essential Oil ofFrontiers in pharmacology · 2021
    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

4 authors at 1 institution in 1 country.

Letizia MezzasomaDepartment of Medicine and Surgery, University of Perugia, 06123 Perugia, Italy.ORCID 0000-0002-6159-0927
Vincenzo Nicola TalesaDepartment of Medicine and Surgery, University of Perugia, 06123 Perugia, Italy.
Rita RomaniDepartment of Medicine and Surgery, University of Perugia, 06123 Perugia, Italy.
Ilaria BellezzaDepartment of Medicine and Surgery, University of Perugia, 06123 Perugia, Italy.ORCID 0000-0002-8106-1600
University of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated inflammasome activation and interleukin (IL)-1β production are associated with several inflammatory disorders. Three different routes can lead to inflammasome activation: a canonical two-step, a non-canonical Caspase-4/5- and Gasdermin D-dependent, and an alternative Caspase-8-mediated pathway. Natriuretic Peptides (NPs), Atrial Natriuretic Peptide (ANP) and B-type Natriuretic Peptide (BNP), binding to Natriuretic Peptide Receptor-1 (NPR-1), signal by increasing cGMP (cyclic guanosine monophosphate) levels that, in turn, stimulate cGMP-dependent protein kinase-I (PKG-I). We previously demonstrated that, by counteracting inflammasome activation, NPs inhibit IL-1β secretion. Here we aimed to decipher the molecular mechanism underlying NPs effects on THP-1 cells stimulated with lipopolysaccharide (LPS) + ATP. Involvement of cGMP and PKG-I were assessed pre-treating THP-1 cells with the membrane-permeable analogue, 8-Br-cGMP, and the specific inhibitor KT-5823, respectively. We found that NPs, by activating NPR-1/cGMP/PKG-I axis, lead to phosphorylation of NLRP3 at Ser295 and to inflammasome platform disassembly. Moreover, by increasing intracellular cGMP levels and activating phosphodiesterases, NPs interfere with both Gasdermin D and Caspase-8 cleavage, indicating that they disturb non-canonical and alternative routes of inflammasome activation. These results showed that ANP and BNP anti-inflammatory and immunomodulatory actions may involve the inhibition of all the known routes of inflammasome activation. Thus, NPs might be proposed for the treatment of the plethora of diseases caused by a dysregulated inflammasome activation.

Indexed as

Adenosine TriphosphateAtrial Natriuretic FactorCaspase 8Cyclic GMPCyclic GMP-Dependent Protein Kinase Type IGasderminsHumansInflammasomesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLipopolysaccharidesNatriuretic Peptide, BrainNLR Family, Pyrin Domain-Containing 3 ProteinPhosphate-Binding ProteinsReceptors, Atrial Natriuretic FactorSignal TransductionAdenosine TriphosphateAtrial Natriuretic Factoratrial natriuretic factor receptor ACaspase 8Cyclic GMPCyclic GMP-Dependent Protein Kinase Type IGasderminsGSDMD protein, humanInflammasomesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLipopolysaccharidesNatriuretic Peptide, BrainNLR Family, Pyrin Domain-Containing 3 ProteinPhosphate-Binding ProteinsReceptors, Atrial Natriuretic FactorcGMP-dependent protein kinaseIL-1βimmune-modulationinflammationNatriuretic Peptide Receptor

Identifiers

PMID33375031
PMCPMC7792787
OpenAlexW3116691810

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.