Evidence map›Paper›PMID 28993096›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2017

Altered expression of MALAT1 lncRNA in nonalcoholic steatohepatitis fibrosis regulates CXCL5 in hepatic stellate cells.

Fatjon Leti, Christophe Legendre, Christopher D Still, Xin Chu, Anthony Petrick, Glenn S Gerhard, Johanna K DiStefano

Abstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
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  11. Long non-coding RNAMolecular therapy. Nucleic acids · 2025
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20 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

Fatjon LetiNational Jewish Health, Denver, Colo.
Christophe LegendreTranslational Genomics Research Institute, Phoenix, Ariz.
Christopher D StillGeisinger Obesity Institute, Danville, Pa.
Xin ChuGeisinger Obesity Institute, Danville, Pa.
Anthony PetrickGeisinger Obesity Institute, Danville, Pa.
Glenn S GerhardTemple University School of Medicine, Philadelphia, Pa.
Johanna K DiStefanoNational Jewish Health, Denver, Colo. Electronic address: distefanoj@njhealth.org.
University of Colorado Denver · USTemple University · USTranslational Genomics Research Institute · US

Funding

Genetic determinants of NAFLD severity and progressionR01DK091601 · NIDDK · TRANSLATIONAL GENOMICS RESEARCH INST · PI DISTEFANO, JOHANNA K, GERHARD, GLENN S · 2011 to 2015
$2.9M
Genetic Determinants of Weight Loss and Resolution of Co-MorbiditiesR01DK088231 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI GERHARD, GLENN S · 2011 to 2015
$2.5M
NIDDK NIH HHS R01 DK088231NIDDK NIH HHS R01 DK091601
6 · The paper itself

Abstract

In the present study, we sought to identify long noncoding RNA (lncRNA) expression profiles in nonalcoholic steatohepatitis (NASH) patients with histologic evidence of lobular inflammation and advanced fibrosis. We profiled lncRNA expression using RNA-sequencing of wedge liver biopsies from 24 nonalcoholic fatty liver disease (NAFLD) patients with normal liver histology, 53 NAFLD patients with lobular inflammation, and 65 NAFLD patients with advanced fibrosis. Transcript profiling identified 4432 and 4057 differentially expressed lncRNAs in comparisons of normal tissue with lobular inflammation and fibrosis samples, respectively. Functional enrichment analysis revealed lncRNA participation in transforming growth factor beta 1 and tumor necrosis factor signaling, insulin resistance, and extracellular matrix maintenance. Several lncRNAs were highly expressed in fibrosis relative to normal tissue, including nuclear paraspeckle assembly transcript 1, hepatocellular carcinoma upregulated lncRNA, and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). Two potential target mRNAs, syndecan 4 (SDC4), and C-X-C motif chemokine ligand 5 (CXCL5) were identified for hepatocellular carcinoma upregulated lncRNA and MALAT1, respectively, but only CXCL5 showed differential expression among the different histologic classes. Knockdown of MALAT1 expression reduced CXCL5 transcript and protein levels by 50% and 30%, respectively, in HepG2 cells. The expression of MALAT1 and CXCL5 was upregulated in activated hepatic stellate (LX-2) cells compared to cells in the quiescent state, and MALAT1 expression was regulated by hyperglycemia and insulin in HepG2 cells, but only by insulin in LX-2 cells. Dysregulated lncRNA expression is associated with inflammation and fibrosis in NASH. Functionally relevant differences in MALAT1 expression may contribute to the development of fibrosis in NASH through mechanisms involving inflammatory chemokines.

Indexed as

Chemokine CXCL5Hepatic Stellate CellsHumansLiver CirrhosisMetabolic Networks and PathwaysNon-alcoholic Fatty Liver DiseaseRNA, Long NoncodingTranscriptomeChemokine CXCL5CXCL5 protein, humanMALAT1 long non-coding RNA, humanRNA, Long Noncoding

Identifiers

PMID28993096
PMCPMC5705449
OpenAlexW2755372191

What OpenQuestion holds

Textmetadata
LicenceTDM
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.