Evidence map›Paper›PMID 25132730›Full record

ArticleMediators of inflammation2014

Macrophage trafficking as key mediator of adenine-induced kidney injury.

Matheus Correa-Costa, Tárcio Teodoro Braga, Raphael José Ferreira Felizardo, Vinícius Andrade-Oliveira, Katia Regina Perez, Iolanda Midea Cuccovia, Meire Ioshie Hiyane, João Santana da Silva, Niels Olsen Saraiva Câmara

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

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  12. Cryptotanshinone Ameliorates Radiation-Induced Lung Injury in Rats.Evidence-based complementary and alternative medicine : eCAM · 2019
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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

9 authors at 2 institutions in 1 country.

Matheus Correa-CostaLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, Brazil.ORCID 0000-0003-3364-4390
Tárcio Teodoro BragaLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, Brazil.
Raphael José Ferreira FelizardoLaboratory of Clinical and Experimental Immunology, Nephrology Division, Federal University of São Paulo, 04023-900 São Paulo, SP, Brazil.
Vinícius Andrade-OliveiraLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, Brazil.
Katia Regina PerezDepartment of Biophysics, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil.ORCID 0000-0001-9612-1816
Iolanda Midea CuccoviaInstitute of Chemistry, Department of Biochemistry, University of São Paulo, 05508-000 São Paulo, SP, Brazil.ORCID 0000-0001-8285-7419
Meire Ioshie HiyaneLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, Brazil.
João Santana da SilvaDepartment of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
Niels Olsen Saraiva CâmaraLaboratory of Transplantation Immunobiology, Department of Immunology, University of São Paulo, Institute of Biomedical Sciences, 05508-900 São Paulo, SP, Brazil ; Laboratory of Clinical and Experimental Immunology, Nephrology Division, Federal University of São Paulo, 04023-900 São Paulo, SP, Brazil.
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. In this sense, tubule interstitial nephritis (TIN) represents an underestimated insult, which can be triggered by different stimuli and, in the absence of a proper regulation, can lead to fibrosis deposition. Based on this perception, we evaluated the participation of macrophage recruitment in the development of TIN. Initially, we provided adenine-enriched food to WT and searched for macrophage presence and action in the kidney. Also, a group of animals were depleted of macrophages with the clodronate liposome while receiving adenine-enriched diet. We collected blood and renal tissue from these animals and renal function, inflammation, and fibrosis were evaluated. We observed higher expression of chemokines in the kidneys of adenine-fed mice and a substantial protection when macrophages were depleted. Then, we specifically investigated the role of some key chemokines, CCR5 and CCL3, in this TIN experimental model. Interestingly, CCR5 KO and CCL3 KO animals showed less renal dysfunction and a decreased proinflammatory profile. Furthermore, in those animals, there was less profibrotic signaling. In conclusion, we can suggest that macrophage infiltration is important for the onset of renal injury in the adenine-induced TIN.

Indexed as

Acute Kidney InjuryAdenineAnimalsChemokine CCL3Flow CytometryKidneyMacrophagesMiceMice, KnockoutNephritis, InterstitialReceptors, CCR5AdenineCCR5 protein, mouseChemokine CCL3Receptors, CCR5

Identifiers

PMID25132730
PMCPMC4124723
OpenAlexW1994835377

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.