Evidence map›Paper›PMID 30783187›Full record

ArticleScientific reports2019

Interleukin 17A promotes diabetic kidney injury.

Jin Ma, Yan J Li, Xiaochen Chen, Tony Kwan, Steven J Chadban, Huiling Wu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 82 citations in OpenAlex.

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  12. Role of Interleukins in Type 1 and Type 2 Diabetes.Diagnostics (Basel, Switzerland) · 2025
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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.

Jin MaKidney Node Laboratory, The Charles Perkins Centre, Sydney Medical School, University of Sydney, Sydney, Australia.
Yan J LiKidney Node Laboratory, The Charles Perkins Centre, Sydney Medical School, University of Sydney, Sydney, Australia.
Xiaochen ChenKidney Node Laboratory, The Charles Perkins Centre, Sydney Medical School, University of Sydney, Sydney, Australia.
Tony KwanKidney Node Laboratory, The Charles Perkins Centre, Sydney Medical School, University of Sydney, Sydney, Australia.
Steven J ChadbanKidney Node Laboratory, The Charles Perkins Centre, Sydney Medical School, University of Sydney, Sydney, Australia.
Huiling WuKidney Node Laboratory, The Charles Perkins Centre, Sydney Medical School, University of Sydney, Sydney, Australia. huiling.wu@sydney.edu.au.
University of Sydney · AURoyal Prince Alfred Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of the pro-inflammatory cytokine IL-17 in the pathogenesis of numerous inflammatory disorders is well-documented, but conflicting results are reported for its role in diabetic nephropathy. Here we examined the role of IL-17 signalling in a model of streptozotocin-induced diabetic nephropathy through IL-17 knockout mice, administration of neutralising monoclonal anti-IL-17 antibody and in vitro examination of gene expression of renal tubular cells and podocytes under high glucose conditions with or without recombinant IL-17. IL-17 deficient mice were protected against progression of diabetic nephropathy, exhibiting reduced albuminuria, glomerular damage, macrophage accumulation and renal fibrosis at 12 weeks and 24 weeks. Administration of anti-IL-17 monoclonal antibody to diabetic wild-type mice was similarly protective. IL-17 deficiency also attenuated up-regulation of pro-inflammatory and pro-fibrotic genes including IL-6, TNF-α, CCL2, CXCL10 and TGF-β in diabetic kidneys. In vitro co-stimulation with recombinant IL-17 and high glucose were synergistic in increasing the expression of pro-inflammatory genes in both cultured renal tubular cells and podocytes. We conclude that absence of IL-17 signalling is protective against streptozotocin-induced diabetic nephropathy, thus implying a pro-inflammatory role of IL-17 in its pathogenesis. Targeting the IL-17 axis may represent a novel therapeutic approach in the treatment of this disorder.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisInterleukin-17KidneyMiceMice, KnockoutIl17a protein, mouseInterleukin-17

Identifiers

PMID30783187
PMCPMC6381173
OpenAlexW2924225396

What OpenQuestion 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 OpenQuestion graph.