Evidence map›Paper›PMID 29230705›Full record

ArticleInternational urology and nephrology2018

Crosstalk between TLR4 and Notch1 signaling in the IgA nephropathy during inflammatory response.

Xuxiang Sheng, Xiaoyan Zuo, Xihui Liu, Yang Zhou, Xia Sun

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Article in International urology and nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  17. Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020
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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

5 authors at 2 institutions in 1 country.

Xuxiang ShengDepartment of Nephrology, Linyi People's Hospital, Linyi, 276003, Shandong, People's Republic of China.
Xiaoyan ZuoDepartment of Nephrology, Yiyuan People's Hospital, Zibo, Shandong, People's Republic of China.
Xihui LiuDepartment of Nephrology, Linyi People's Hospital, Linyi, 276003, Shandong, People's Republic of China. liuxihui0909@126.com.
Yang ZhouDepartment of Nephrology, Affiliated Hospital of Ningbo University Medical School, Ningbo, Zhejiang, People's Republic of China.
Xia SunDepartment of Nephrology, Linyi People's Hospital, Linyi, 276003, Shandong, People's Republic of China.
Linyi People's Hospital · CNNingbo University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIgA nephropathy (IgAN) is an immune complex-mediated disease involved in the kidney disease. Recent studies have revealed that Notch signaling-related genes are aberrantly expressed in various cell types and maybe associate with inflammation-induced carcinogenesis. The aim of our study was to investigate the function of Notch1 in the inflammatory response of IgAN.

methodsThe expression of Notch1, Jagged1 and NICD1 in 52 IgAN renal tissues and 20 control renal tissues was first determined using quantitative real-time PCR and Western blot. ELISA was then used to estimate the inflammatory response of human podocytes to LPS. NF-κB activity was measured using dual-luciferase reporter assay. Activation of Notch1 and NF-κB signaling pathway was assessed using Western blot.

resultsThe expression of Notch1, NICD1 and Jagged1 was significantly higher in IgAN renal tissues than control renal tissues (P < 0.05). LPS treatment resulted in an obvious increase of MCP-1, IL-8 and phosphorylated NF-κB p65 in podocytes polymeric IgA (pIgA) IgAN group compared to control group (P < 0.05 for all). Activated Notch1 and its target genes, Hes1 and Hey1 were also enhanced upon LPS stimulation. Silencing of Notch1 signaling with inhibitor DAPT, NF-κB activation and LPS-induced inflammatory response were obviously attenuated, whereas Notch1 activator Jagged1 could markedly restore NF-κB activity and LPS-induced inflammatory response (P < 0.05 for all).

conclusionsCrosstalk between TLR4 and Notch1 signaling regulates the inflammatory response in the IgAN and maybe plays an important role in the progression of IgAN.

Indexed as

AdolescentAdultBasic Helix-Loop-Helix ProteinsCase-Control StudiesCell Cycle ProteinsCells, CulturedChemokine CCL2FemaleGene ExpressionGlomerulonephritis, IGAHumansImmunoglobulin AInflammationInterleukin-8Jagged-1 ProteinLipopolysaccharidesBasic Helix-Loop-Helix ProteinsCCL2 protein, humanCell Cycle ProteinsChemokine CCL2CXCL8 protein, humanHES1 protein, humanHEY1 protein, humanImmunoglobulin AInterleukin-8Jagged-1 ProteinLipopolysaccharidesNOTCH1 protein, humanReceptor, Notch1TLR4 protein, humanToll-Like Receptor 4Transcription Factor HES-1Transcription Factor RelAIgA nephropathyInnate immunityNotch1Toll-like receptor 4

Identifiers

PMID29230705
OpenAlexW2772933016

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.