Evidence mapPaperPMID 32229588Full record

ArticleJournal of lipid research2020

The lncRNA Gm15622 stimulates SREBP-1c expression and hepatic lipid accumulation by sponging the miR-742-3p in mice.

Minjuan Ma, Rui Duan, Lulu Shen, Mengting Liu, Yaya Ji, Hao Zhou, Changxian Li, Tingming Liang, Xiangcheng Li, Li Guo

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  8. Targeting Metabolism: Innovative Therapies for MASLD Unveiled.International journal of molecular sciences · 2025
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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

10 authors at 3 institutions in 1 country.

Minjuan MaJiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Science, Nanjing Normal University, Nanjing 210023, China.
Rui DuanJiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Science, Nanjing Normal University, Nanjing 210023, China.
Lulu ShenJiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Science, Nanjing Normal University, Nanjing 210023, China.
Mengting LiuJiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Science, Nanjing Normal University, Nanjing 210023, China.
Yaya JiJiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Science, Nanjing Normal University, Nanjing 210023, China.
Hao ZhouChangzhou Institute of Innovation and Development, Nanjing Normal University, Nanjing 210023, China.
Changxian LiHepatobiliary Center, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Tingming LiangJiangsu Key Laboratory for Molecular and Medical Biotechnology, School of Life Science, Nanjing Normal University, Nanjing 210023, China; Changzhou Institute of Innovation and Development, Nanjing Normal University, Nanjing 210023, China. Electronic address: mailto:tmliang@njnu.edu.cn.
Xiangcheng LiHepatobiliary Center, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Li GuoDepartment of Bioinformatics, School of Geographic and Biologic Information, Nanjing University of Posts and Telecommunications, Nanjing 210023, China.
Nanjing Normal University · CNJiangsu Province Hospital · CNNanjing University of Posts and Telecommunications · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive lipid deposition is a hallmark of NAFLD. Although much has been learned about the enzymes and metabolites involved in NAFLD, few studies have focused on the role of long noncoding RNAs (lncRNAs) in hepatic lipid accumulation. Here, using in vitro and in vivo models of NAFLD, we found that the lncRNA Gm15622 is highly expressed in the liver of obese mice fed a HFD and in murine liver (AML-12) cells treated with free fatty acids. Investigating the molecular mechanism in the liver-enriched expression of Gm15622 and its effects on lipid accumulation in hepatocytes and on NAFLD pathogenesis, we found that Gm15622 acts as a sponge for the microRNA miR-742-3p. This sponging activity increased the expression of the transcriptional regulator SREBP-1c and promoted lipid accumulation in the liver of the HFD mice and AML-12 cells. Moreover, further results indicated that metformin suppresses Gm15622 and alleviates NAFLD-associated lipid deposition in mice. In conclusion, we have identified an lncRNA Gm15622/miR-742-3p/SREBP-1c regulatory circuit associated with NAFLD in mice, a finding that significantly advances our insight into how lipid metabolism and accumulation are altered in this metabolic disorder. Our results also suggest that Gm15622 may be a potential therapeutic target for managing NAFLD.

Indexed as

Gene Expression RegulationAnimalsCell LineLipid MetabolismLiverMiceRNA, Long NoncodingSterol Regulatory Element Binding Protein 1RNA, Long NoncodingSterol Regulatory Element Binding Protein 1epigenetic regulationfatty acid synthasegene regulationlong noncoding ribonucleic acidmetforminmicro-ribonucleic acidmiR-742-3pnonalcoholic fatty liver diseaseobesitysterol regulatory element-binding protein 1c

Identifiers

PMID32229588
PMCPMC7328049
OpenAlexW3013520266

What Socratic 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 Socratic graph.