Evidence map›Paper›PMID 26887957›Full record

ArticleScientific reports2016

Liver X receptor α is essential for the capillarization of liver sinusoidal endothelial cells in liver injury.

Yan Xing, Tingting Zhao, Xiaoyan Gao, Yuzhang Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
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  7. Integrative analysis reveals multiple modes of LXR transcriptional regulation in liver.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Liver X receptors and liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  10. Review
  11. The roles and mechanisms of hypoxia in liver fibrosis.Journal of translational medicine · 2021
    Review
  12. Review
  13. Review
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  15. The wHole Story About Fenestrations in LSEC.Frontiers in physiology · 2021
    Review
  16. 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

4 authors at 1 institution in 1 country.

Yan XingInstitute of Immunology, PLA, Third Military Medical University, Chongqing, 400038, PR China.
Tingting ZhaoInstitute of Immunology, PLA, Third Military Medical University, Chongqing, 400038, PR China.
Xiaoyan GaoInstitute of Immunology, PLA, Third Military Medical University, Chongqing, 400038, PR China.
Yuzhang WuInstitute of Immunology, PLA, Third Military Medical University, Chongqing, 400038, PR China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver X receptors (LXRs) play essential roles in lipogenesis, anti-inflammatory action and hepatic stellate cells (HSCs) activation in the liver. However, the effects of LXRs on the capillarization of liver sinusoidal endothelial cells (LSECs) in liver fibrosis remain undetermined. Here, we demonstrated that LXRα plays an important role in LSECs capillarization in a manner that involved Hedgehog (Hh) signaling. We found that LXRα expression in LSECs was increased in the carbon tetrachloride (CCl4)-induced fibrosis model. LXRα deletion markedly exacerbated CCl4-induced lesions assessed by histopathology, as well as inflammation and collagen deposition. Furthermore, capillarization of the sinusoids was aggravated in CCl4 -treated LXRα-deficient mice, as evidenced by increased CD34 expression, the formation of continuous basement membranes and aggravation of the loss of fenestrae. In vitro, LXR agonist could maintain freshly isolated LSECs differentiation on day 3. Furthermore, LXRα deletion led to increased expression of Hedgehog (Hh)-regulated gene in LSECs in the injured liver. Conversely, the LXR agonist could inhibit the Hh pathway in cultured LSECs. These responses indicated that LXRα suppressed the process of LSECs capillarization by repressing Hh signaling. Overall, our findings suggest that LXRα, by restoring the differentiation of LSECs, may be critical for the regression of liver fibrosis.

Indexed as

Signal TransductionAnimalsCapillariesCarbon Tetrachloride PoisoningEndothelial CellsHedgehog ProteinsHepatic Stellate CellsLiverLiver CirrhosisLiver X ReceptorsMaleMiceMice, KnockoutHedgehog ProteinsLiver X Receptors

Identifiers

PMID26887957
PMCPMC4758044
OpenAlexW2295816037

What OpenQuestion holds

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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.