Evidence mapPaperPMID 27614743Full record

ArticleClinical and experimental nephrology2017

Clarithromycin attenuates the expression of monocyte chemoattractant protein-1 by activating toll-like receptor 4 in human mesangial cells.

Koji Tsugawa, Tadaatsu Imaizumi, Shojiro Watanabe, Kazushi Tsuruga, Hidemi Yoshida, Hiroshi Tanaka

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In one paragraph

Article in Clinical and experimental nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. International journal of nanomedicine · 2024
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  3. Review
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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

6 authors at 2 institutions in 1 country.

Koji TsugawaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki University, Hirosaki, 036-8563, Japan.
Tadaatsu ImaizumiDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki University, Hirosaki, 036-8562, Japan.
Shojiro WatanabeDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki University, Hirosaki, 036-8563, Japan.
Kazushi TsurugaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki University, Hirosaki, 036-8563, Japan.
Hidemi YoshidaDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki University, Hirosaki, 036-8562, Japan.
Hiroshi TanakaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki University, Hirosaki, 036-8563, Japan. hirotana@hirosaki-u.ac.jp.ORCID http://orcid.org/0000-0001-7057-813X
Hirosaki University · JPHirosaki University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSignaling pathways induced by the activation of renal toll-like receptor 4 (TLR4) play a pivotal role in chronic kidney disease (CKD). Some recent studies suggested that clarithromycin (CAM), a 14-membered ring macrolide, exerts renoprotective effects by suppressing proinflammatory chemokines. However, its beneficial effects on signaling pathways through renal TLR4 activation are unknown.

methodsCultured human mesangial cells (MCs) were treated with lipopolysaccharide (LPS). Expression of monocyte chemoattractant protein-1 (MCP-1/CCL2) and interleukin-8 (IL-8/CXCL8) was analyzed by quantitative RT-PCR and enzyme-linked immunosorbent assay. Signaling pathways affected by CAM were determined by examining the activation of nuclear factor-κB (NF-κB) and p38 mitogen-activated protein kinase (MAPK) by performing western blotting.

resultsCAM inhibited both the mRNA and protein expression of MCP-1 without cell injury but did not affect those expressions of IL-8 in LPS-stimulated MCs. Interestingly, CAM decreased p38 MAPK activation by inhibiting phosphorylation but did not affect NF-κB activation.

conclusionOur results indicated that CAM exerted renoprotective effects by suppression of p38 MAPK activity and by decreasing the expression of MCP-1 in LPS-stimulated MCs. Given the implication of TLR4 signaling in CKD, CAM may be a potential treatment of choice for CKD.

Indexed as

Cells, CulturedChemokine CCL2ClarithromycinCytoprotectionDose-Response Relationship, DrugDown-RegulationHumansLipopolysaccharidesMAP Kinase Kinase KinasesMesangial Cellsp38 Mitogen-Activated Protein KinasesPhosphorylationProtective AgentsSignal TransductionToll-Like Receptor 4CCL2 protein, humanChemokine CCL2ClarithromycinLipopolysaccharidesMAP Kinase Kinase Kinasesp38 Mitogen-Activated Protein KinasesProtective AgentsTLR4 protein, humanToll-Like Receptor 4ClarithromycinMesangial cellsMonocyte chemoattractant protein-1Toll-like receptor 4

Identifiers

PMID27614743
OpenAlexW2514181989

What Socratic holds

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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 Socratic graph.