Evidence map›Paper›PMID 34651657›Full record

ArticleInternational journal of molecular medicine2021

MALAT1 promotes liver fibrosis by sponging miR‑181a and activating TLR4‑NF‑κB signaling.

Yinghui Wang, Qiuju Mou, Zixin Zhu, Luqiang Zhao, Lili Zhu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Review
  2. Tropical medicine and infectious disease · 2026
    Article
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  7. Article
  8. Article
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  11. Long non-coding RNAMolecular therapy. Nucleic acids · 2025
    Review
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  13. Article
  14. Review
  15. Article
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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 2 institutions in 1 country.

Yinghui Wang *School of Clinical Laboratory Science, Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Qiuju Mou *Department of Blood Transfusion, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Zixin ZhuDepartment of Basic Medical College, Guizhou Medical University, Guiyang, Guizhou 550025, P.R. China.
Luqiang ZhaoSchool of Clinical Laboratory Science, Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Lili ZhuSchool of Clinical Laboratory Science, Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Guiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate whether long non‑coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) could modulate activation and inflammation of hepatic stellate cell (HSCs) via regulation of a microRNA (miR)‑181a‑toll like receptor (TLR)4/nuclear factor (NF)‑κB axis, thereby contributing to the development of liver fibrosis. A total of 151 patients with liver fibrosis were recruited, and the serum levels of alanine transaminase, aspartate aminotransferase and albumin were determined. Transforming growth factor (TGF)‑β1 and LPS were used to activate and induce inflammation in the human HSC cell line LX2. MALAT1 was knocked using small interfering RNA or overexpressed, and an inhibitor and mimic of miR‑181a‑5p were used to examine the effect of MALAT1 and miR‑181a‑5p on the activation and inflammation of LX2 cells. Both MALAT1 and miR‑181a‑5p expression performed well in their ability to differentiate patients with liver fibrosis from healthy volunteers, and MALAT1 expression was associated with the severity of liver fibrosis. The expression levels of TLR4 and NF‑κB were increased after stimulation with LPS or TGF‑β1, but MALAT1 knockdown or miR‑181a‑5p mimic transfection abrogated this increase. Moreover, the TGF‑β1‑induced increase in viability, proliferation, migration, adhesion and collagen production, and the LPS‑induced inflammation of LX2 cells were all reversed after MALAT1 knockdown or transfection with miR‑181a‑5p mimic. The MALAT1/miR‑181a‑5p axis was involved in regulating collagen production and inflammation by activating TLR4/NF‑κB signaling, which may be conducive to liver fibrosis treatment in the future.

Indexed as

AdultAgedCase-Control StudiesCell AdhesionCell MovementCell ProliferationCollagenFemaleGene Expression RegulationHepatic Stellate CellsHumansLiver CirrhosisMaleMicroRNAsMiddle AgedNF-kappa BCollagenMALAT1 long non-coding RNA, humanMicroRNAsMIrn181 microRNA, humanNF-kappa BRNA, Long NoncodingTLR4 protein, humanToll-Like Receptor 4collagen productiondiagnosisinflammationlipopolysaccharideliver fibrosislong non‑coding RNA metastasis associated lung adenocarcinoma transcript 1microRNA‑181a‑5ptransforming growth factor‑β1

Identifiers

PMID34651657
PMCPMC8547543
OpenAlexW3206460155

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.