Evidence map›Paper›PMID 24357263›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2014

Kinin B1 receptor deficiency attenuates cisplatin-induced acute kidney injury by modulating immune cell migration.

Gabriel R Estrela, Frederick Wasinski, Danilo C Almeida, Mariane T Amano, Angela Castoldi, Carolina C Dias, Denise M A C Malheiros, Sandro S Almeida, Edgar J Paredes-Gamero, João B Pesquero and 3 more

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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Kinin BPharmaceutics · 2023
    Article
  4. Renal fibrosis due to multiple cisplatin treatment is exacerbated by kinin B1 receptor antagonism.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  5. Article
  6. Kinin B1 Receptor Is Important in the Pathogenesis of Myeloperoxidase-Specific ANCA GN.Journal of the American Society of Nephrology : JASN · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Kidney tubules: intertubular, vascular, and glomerular cross-talk.Current opinion in nephrology and hypertension · 2016
    Review
  13. Article
  14. 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

13 authors at 4 institutions in 1 country.

Gabriel R EstrelaDepartamento de Biofísica, Universidade Federal de São Paulo, São Paulo, Brazil.
Frederick Wasinski
Danilo C Almeida
Mariane T Amano
Angela Castoldi
Carolina C Dias
Denise M A C Malheiros
Sandro S Almeida
Edgar J Paredes-Gamero
João B Pesquero
Carlos C Barros
Niels O S Câmara
Ronaldo C Araújo
Universidade Federal de São Paulo · BRUniversidade de São Paulo · BRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRUniversidade Federal de Pelotas · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledCisplatin is a chemotherapeutic agent that causes severe renal dysfunction. The kinin B1 receptor has been associated with the migration of immune cells to injured tissue as well as with renal inflammation. To examine the role of the kinin B1 receptor in cisplatin-induced acute kidney injury, we used kinin B1 receptor knockout mice and treatment with a receptor antagonist before and after cisplatin administration. Cisplatin injection caused exacerbation of renal macrophage and neutrophil migration, higher levels of serum creatinine and blood urea, upregulation of B1 receptor mRNA and an increase in pro-inflammatory cytokines expression. B1 receptor knockout mice exhibited a reduction in serum creatinine and blood urea levels, diminished apoptosis, and decreased cisplatin-induced upregulation of inflammatory components. Moreover, treatment with the B1 receptor antagonist prior to cisplatin administration normalized serum creatinine, blood urea levels, protected from acute tubular necrosis, apoptosis-related genes, and prevented upregulation of pro-inflammatory cytokines. Thus, we propose that kinins have an important role in cisplatin-induced acute kidney injury by impairing immune cells migration to renal tissue during cisplatin nephrotoxicity. KEY MESSAGE: Kinin B1 receptor is upregulated after cisplatin exposure. Kinin B1 receptor deficiency diminishes the nephrotoxicity caused by cisplatin. Kinin B1 receptor deficiency ameliorates the inflammatory response. Kinin B1 receptor deficiency diminishes apoptosis caused by cisplatin. Kinin B1 receptor antagonism ameliorates renal function after cisplatin injection.

Indexed as

Cell MovementAcute Kidney InjuryAnimalsAntineoplastic AgentsApoptosisBlood Urea NitrogenBradykininBradykinin B1 Receptor AntagonistsCell ProliferationCisplatinCreatinineCytokinesKidneyMacrophagesMaleMice, Inbred C57BLAntineoplastic AgentsBradykininBradykinin B1 Receptor AntagonistsCisplatinCreatinineCytokinesR 715Receptor, Bradykinin B1

Identifiers

PMID24357263
OpenAlexW2148151353

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.