Evidence map›Paper›PMID 28861170›Full record

ArticleAmerican journal of translational research2017

MiR-663a/MiR-423-5p are involved in the pathogenesis of lupus nephritis via modulating the activation of NF-κB by targeting TNIP2.

Weisong Wang, Junjie Gao, Fangli Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Weisong WangDepartment of Nephrology, Cangzhou Central HospitalCangzhou 061001, China.
Junjie GaoDepartment of Nephrology, Cangzhou Central HospitalCangzhou 061001, China.
Fangli WangDepartment of Nephrology, Cangzhou Central HospitalCangzhou 061001, China.
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lupus nephritis (LN) is a kidney disorder resulting from systemic lupus erythematosus (SLE), an autoimmune inflammatory disease. MicroRNAs (miRNAs) have emerged as a new class of therapeutic targets in LN treatment, but how they specifically contribute to the disease development remains unknown. In this study, the expression of miR-663a/miR-423-5p and TNIP2 were compared between human renal biopsy tissues from LN patients and renal cell carcinoma patients. Additionally, the LN mouse model was used to measure the levels of miR-663a/miR-423-5p and TNIP2 in the control group and the experiment group. Dual luciferase reporter assay was used to validate TNIP2 as the target of miR-663a/miR-423-5p. MiR-663a/miR-423-5p were highly expressed in kidney tissues from LN patients as compared to kidney tissues from SLE patients and normal tissues. TNIP2 showed comparatively low expression in tissues from LN patients. In the LN mouse model, the levels of miR-663a/miR-423-5p were improved whereas TNIP2 was reduced in response to renal injury stimulated by pristine. MiR-663a/miR-423-5p mimics and inhibitors triggered decrease and increase of TNIP2 levels, respectively. Dual luciferase assay showed that TNIP2 was a direct target of miR-663a/miR-423-5p. In addition, detection of inflammatory factors confirmed that miR-663a/miR-423-5p and TNIP2 fundamentally contributed to LPS-induced NF-κB activation. Our findings suggested the involvement of miR-663a/miR-423-5p-TNIP2-NF-κB axis in the development of LN, thereby providing new therapeutic targets for LN treatment.

Indexed as

inflammatorylupus nephritismiR-663a/miR-423-5pNF-κBTNIP2

Identifiers

PMID28861170
PMCPMC5575193
OpenAlexW2944161999

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.