Evidence map›Paper›PMID 33505165›Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021

Downregulation of lncRNA EPB41L4A-AS1 Mediates Activation of MYD88-Dependent NF-κB Pathway in Diabetes-Related Inflammation.

Ziqing Wang, Weijie Liao, Fuhai Liu, Tingpeng Yang, Weidong Xie, Meijian Liao, Dayong Gu, Yaou Zhang

Open access · goldAbstract read
In one paragraph

Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

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  11. Long Noncoding RNAs in the Pathogenesis of Insulin Resistance.International journal of molecular sciences · 2022
    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

8 authors at 3 institutions in 1 country.

Ziqing WangSchool of Chemistry, Tsinghua University, Beijing 100084, People's Republic of China.
Weijie LiaoState Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Shenzhen 518055, People's Republic of China.
Fuhai LiuState Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Shenzhen 518055, People's Republic of China.
Tingpeng YangState Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Shenzhen 518055, People's Republic of China.
Weidong XieState Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Shenzhen 518055, People's Republic of China.
Meijian LiaoKey Laboratory in Healthy Science and Technology, Division of Life Science, Tsinghua Shenzhen International Graduate School, Shenzhen 518055, People's Republic of China.
Dayong GuDepartment of Laboratory Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen 518035, People's Republic of China.
Yaou ZhangState Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Shenzhen 518055, People's Republic of China.
Xuzhou Medical College · CNShenzhen Second People's Hospital · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLong non-coding RNAs (lncRNAs) have been shown to be involved in many human diseases. In this study, we aimed to reveal the role and molecular mechanism of lncRNA EPB41L4A-AS1 in type 2 diabetic mellitus (T2DM)-related inflammation.

methodsTo explore the relationships between the expression of EPB41L4A-AS1 and inflammatory factors in the blood of T2DM patients, we analyzed peripheral blood mononuclear cell (PBMC) expression microarrays of T2DM patients and expression microarrays of PBMC treated with lipopolysaccharide (LPS) from the GEO database. The relationship between EPB41L4A-AS1 and phospho-p65 was explored by Western blotting (WB) and immunofluorescence. The interactions between EPB41L4A-AS1 and myeloid differentiation factor 88 (MYD88) were also verified through quantitative real-time PCR, WB, and chromatin immunoprecipitation. Glycolysis and mitochondrial stress were detected by Seahorse.

resultsEPB41L4A-AS1 showed very low expression, which was significantly negatively correlated with levels of inflammatory factors in PBMCs of T2DM patients and PBMCs treated with LPS. These results were verified by cell experiments on PBMC and THP-1 cells. Knockdown of EPB41L4A-AS1 led to the phosphorylation and nuclear translocation of p65 and thus activated the NF-κB signaling pathway; it also reduced the enrichment of H3K9me3 in the

conclusionEPB41L4A-AS1 knockdown activated the NF-κB signaling pathway through a MYD88-dependent regulatory mechanism, promoted glycolysis, and ultimately enhanced the inflammatory response. These results demonstrate that EPB41L4A-AS1 is closely associated with inflammation in T2DM, and that low expression of EPB41L4A-AS1 may be used as an indicator of chronic inflammation and possible diabetic vascular complications in T2DM patients.

Indexed as

diabetesEPB41L4A-AS1inflammationMYD88NF-κB

Identifiers

PMID33505165
PMCPMC7829128
OpenAlexW3122320257

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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.