Evidence map›Paper›PMID 31961061›Full record

ArticleJournal of cellular and molecular medicine2020

Epigenetic silencing of LncRNA ANRIL enhances liver fibrosis and HSC activation through activating AMPK pathway.

Jing-Jing Yang, Yang Yang, Chong Zhang, Jun Li, Yan Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  13. [A study of the anti-fibrotic effect of ghrelin on mice with nonalcoholic steatohepatitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
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  16. Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023
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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 1 institution in 1 country.

Jing-Jing YangDepartment of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei, China.
Yang YangDepartment of Surgical Oncology, The Affiliated Suzhou Science & Technology Town Hospital of Nanjing Medical University, Suzhou, China.
Chong ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei, China.
Jun LiSchool of Pharmacy, Anhui Medical University, Hefei, China.ORCID 0000-0002-9019-8561
Yan YangDepartment of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei, China.
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (LncRNAs) and DNA methylation are important epigenetic mark play a key role in liver fibrosis. Currently, how DNA methylation and LncRNAs control the hepatic stellate cell (HSC) activation and fibrosis has not yet been fully characterized. Here, we explored the role of antisense non-coding RNA in the INK4 locus (ANRIL) and DNA methylation in HSC activation and fibrosis. The expression levels of DNA methyltransferases 3A (DNMT3A), ANRIL, α-Smooth muscle actin (α-SMA), Type I collagen (Col1A1), adenosine monophosphate-activated protein kinase (AMPK) and p-AMPK in rat and human liver fibrosis were detected by immunohistochemistry, qRT-PCR and Western blotting. Liver tissue histomorphology was examined by haematoxylin and eosin (H&E), Sirius red and Masson staining. HSC was transfected with DNMT3A-siRNA, over-expressing ANRIL and down-regulating ANRIL. Moreover, cell proliferation ability was examined by CCK-8, MTT and cell cycle assay. Here, our study demonstrated that ANRIL was significantly decreased in activated HSC and liver fibrosis tissues, while Col1A1, α-SMA and DNMT3A were significantly increased in activated HSC and liver fibrosis tissues. Further, we found that down-regulating DNMT3A expression leads to inhibition of HSC activation. Reduction in DNMT3A elevated ANRIL expression in activated HSC. Furthermore, we performed the over expression ANRIL suppresses HSC activation and AMPK signalling pathways. In sum, our study found that epigenetic DNMT3A silencing of ANRIL enhances liver fibrosis and HSC activation through activating AMPK pathway. Targeting epigenetic modulators DNMT3A and ANRIL, and offer a novel approach for liver fibrosis therapy.

Indexed as

AMP-Activated Protein KinasesAnimalsCell CycleCell ProliferationCells, CulturedDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3ADown-RegulationEpigenesis, GeneticHepatic Stellate CellsHumansLiverLiver CirrhosisRatsRats, Sprague-DawleyAMP-Activated Protein KinasesANRIL long non-coding RNA, ratDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanRNA, Long NoncodingRNA, Small Interferingantisense non-coding RNA in the INK4 locusDNA methyltransferases 3Aepigenetichepatic stellate cellliver fibrosis

Identifiers

PMID31961061
PMCPMC7028869
OpenAlexW3002160382

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.