Evidence map›Paper›PMID 33090288›Full record

ArticleCellular and molecular life sciences : CMLS2021

Arid2-IR promotes NF-κB-mediated renal inflammation by targeting NLRC5 transcription.

Puhua Zhang, Chaolun Yu, Jianwen Yu, Zhijian Li, Hui-Yao Lan, Qin Zhou

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. METTL3-driven mFrontiers in immunology · 2026
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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 2 countries.

Puhua Zhang *Department of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Zhongshan Road II, Guangzhou, 510080, Guangdong, China.
Chaolun Yu *Department of Endocrinology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong, China.
Jianwen Yu *Department of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Zhongshan Road II, Guangzhou, 510080, Guangdong, China.
Zhijian LiDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Zhongshan Road II, Guangzhou, 510080, Guangdong, China.
Hui-Yao LanDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, 999077, China.
Qin ZhouDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Zhongshan Road II, Guangzhou, 510080, Guangdong, China. zhouqin3@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-7205-082X
Sun Yat-sen University · CNChinese University of Hong Kong · HK

Funding

Guangzhou Science, Technology and Innovation Commission 201806010123Kelin Young Talents Program of the First Affiliated Hospital of Sun Yat-sen University Y50179Natural Science Foundation of Guangdong Province 2020A1515010247The Guangdong-Hong Kong-Macao-Joint Labs Program from Guangdong Science and Technology Department 2019B121205005The Health and Medical Research Fund of Hong Kong 14152321The Health and Medical Research Fund of Hong Kong HMRF 05161326
6 · The paper itself

Abstract

Increasing evidence shows that long non-coding RNAs (lncRNAs) play an important role in a variety of disorders including kidney diseases. It is well recognized that inflammation is the initial step of kidney injury and is largely mediated by nuclear factor Kappa B (NF-κB) signaling. We had previously identified lncRNA-Arid2-IR is an inflammatory lncRNA associated with NF-κB-mediated renal injury. In this study, we examined the regulatory mechanism through which Arid2-IR activates NF-κB signaling. We found that Arid2-IR was differentially expressed in response to various kidney injuries and was induced by transforming growth factor beta 1(TGF-β1). Using RNA sequencing and luciferase assays, we found that Arid2-IR regulated the activity of NF-κB signal via NLRC5-dependent mechanism. Arid2-IR masked the promoter motifs of NLRC5 to inhibit its transcription. In addition, during inflammatory response, Filamin A (Flna) was increased and functioned to trap Arid2-IR in cytoplasm, thereby preventing its nuclear translocation and inhibition of NLRC5 transcription. Thus, lncRNA Arid2-IR mediates NF-κB-driven renal inflammation via a NLRC5-dependent mechanism and targeting Arid2-IR may be a novel therapeutic strategy for inflammatory diseases in general.

Indexed as

Transcription, GeneticAnimalsCells, CulturedDisease Models, AnimalGene Expression ProfilingGene Expression RegulationHEK293 CellsHumansInflammationIntracellular Signaling Peptides and ProteinsKidneyKidney DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutIntracellular Signaling Peptides and ProteinsNF-kappa BNLRC5 protein, mouseRNA, Long NoncodingTransforming Growth Factor beta1Arid2-IRFlnaInflammationNF-κBNLRC5

Identifiers

PMID33090288
PMCPMC11072509
OpenAlexW3093928808

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.