Evidence map›Paper›PMID 26103560›Full record

ArticleBritish journal of pharmacology2016

Inflammasome activity is essential for one kidney/deoxycorticosterone acetate/salt-induced hypertension in mice.

S M Krishnan, J K Dowling, Y H Ling, H Diep, C T Chan, D Ferens, M M Kett, A Pinar, C S Samuel, A Vinh and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

  1. Pooled it
  2. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Epithelial Na+ Channels, Immune Cells, and Salt.Annual review of physiology · 2025
    Review
  14. C-reactive protein promotes diabetic kidney disease via Smad3-mediated NLRP3 inflammasome activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

57 more citing papers are in PubMed but not listed here.

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

19 authors at 7 institutions in 5 countries.

S M KrishnanDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
J K DowlingCentre for Innate Immunity and Infectious Diseases, MIMR-PHI Institute of Medical Research, Clayton, Vic., Australia.
Y H LingDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
H DiepDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
C T ChanDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
D FerensDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
M M KettDepartment of Physiology, Monash University, Clayton, Vic., Australia.
A PinarCentre for Innate Immunity and Infectious Diseases, MIMR-PHI Institute of Medical Research, Clayton, Vic., Australia.
C S SamuelDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
A VinhDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
T V ArumugamDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
T D HewitsonDepartment of Nephrology, Royal Melbourne Hospital, Parkville, Vic., Australia.
B K Kemp-HarperDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
A A B RobertsonDivision of Chemistry and Structural Biology, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
M A CooperDivision of Chemistry and Structural Biology, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
E LatzInstitute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany.
A MansellCentre for Innate Immunity and Infectious Diseases, MIMR-PHI Institute of Medical Research, Clayton, Vic., Australia.
C G SobeyDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
G R DrummondDepartment of Pharmacology, Monash University, Clayton, Vic., Australia.
Monash University · AUHudson Institute of Medical Research · AUUniversity of Queensland · AUMonash Medical Centre · AUNational University of Singapore · SGThe Royal Melbourne Hospital · AUUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeInflammasomes are multimeric complexes that facilitate caspase-1-mediated processing of the pro-inflammatory cytokines IL-1β and IL-18. Clinical hypertension is associated with renal inflammation and elevated circulating levels of IL-1β and IL-18. Therefore, we investigated whether hypertension in mice is associated with increased expression and/or activation of the inflammasome in the kidney, and if inhibition of inflammasome activity reduces BP, markers of renal inflammation and fibrosis. EXPERIMENTAL APPROACH: Wild-type and inflammasome-deficient ASC(-/-) mice were uninephrectomized and received deoxycorticosterone acetate and saline to drink (1K/DOCA/salt). Control mice were uninephrectomized but received a placebo pellet and water. BP was measured by tail cuff; renal expression of inflammasome subunits and inflammatory markers was measured by real-time PCR and immunoblotting; macrophage and collagen accumulation was assessed by immunohistochemistry. KEY

results1K/DOCA/salt-induced hypertension in mice was associated with increased renal mRNA expression of inflammasome subunits NLRP3, ASC and pro-caspase-1, and the cytokine, pro-IL-1β, as well as protein levels of active caspase-1 and mature IL-1β. Following treatment with 1K/DOCA/salt, ASC(-/-) mice displayed blunted pressor responses and were also protected from increases in renal expression of IL-6, IL-17A, CCL2, ICAM-1 and VCAM-1, and accumulation of macrophages and collagen. Finally, treatment with a novel inflammasome inhibitor, MCC950, reversed hypertension in 1K/DOCA/salt-treated mice. CONCLUSIONS AND IMPLICATIONS: Renal inflammation, fibrosis and elevated BP induced by 1K/DOCA/salt treatment are dependent on inflammasome activity, highlighting the inflammasome/IL-1β pathway as a potential therapeutic target in hypertension.

Indexed as

AnimalsApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsDesoxycorticosteroneHypertensionInflammasomesKidney DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutSaltsApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsDesoxycorticosteroneInflammasomesPycard protein, mouseSalts

Identifiers

PMID26103560
PMCPMC4742291
OpenAlexW1608457896

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.