Evidence map›Paper›PMID 35194023›Full record

ArticleCell death discovery2022

Long noncoding RNA SNHG1 silencing accelerates hepatocyte-like cell differentiation of bone marrow-derived mesenchymal stem cells to alleviate cirrhosis via the microRNA-15a/SMURF1/UVRAG axis.

Jia Sun, Xuedong Sun, Sean Hu, Maoqiang Wang, Na Ma, Junhui Chen, Feng Duan

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Role of noncoding RNAs in liver fibrosis.World journal of gastroenterology · 2023
    Review
  6. Review
  7. Article
  8. Article
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.

Jia Sun *Shenzhen Beike Biotechnology Research Institute, Shenzhen, 518057, P.R. China.
Xuedong Sun *Department of Interventional Radiology, the First Medical Center, Chinese PLA General Hospital, Beijing, 100853, P.R. China.
Sean HuShenzhen Beike Biotechnology Research Institute, Shenzhen, 518057, P.R. China.
Maoqiang WangDepartment of Interventional Radiology, the First Medical Center, Chinese PLA General Hospital, Beijing, 100853, P.R. China.
Na MaDepartment of Radiotherapy, the First Medical Center, Chinese PLA General Hospital, Beijing, 100853, P.R. China.
Junhui ChenIntervention and Cell Therapy Center, Shenzhen Hospital of Peking University, Shenzhen, 518057, P. R. China.
Feng DuanDepartment of Interventional Radiology, the First Medical Center, Chinese PLA General Hospital, Beijing, 100853, P.R. China. duanfeng@vip.sina.com.ORCID http://orcid.org/0000-0002-8089-2963
Chinese PLA General Hospital · CNBeike Biotechnology (China) · CNPeking University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow-derived mesenchymal stem cells (BMSCs) can differentiate into hepatocyte-like cells (HLCs) to attenuate cirrhosis. Long noncoding RNA (lncRNA) SNHG1 has been demonstrated to orchestrate BMSC differentiation, whereas its role in cirrhosis remains elusive. Therefore, this study was performed to figure out whether lncRNA SNHG1 was involved in cirrhosis by affecting HLC differentiation of BMSCs. Mouse BMSCs were isolated, and the BMSC differentiation into HLCs was induced by hepatocyte growth factor (HGF). A cirrhotic mouse model was established using carbon tetrachloride and phenobarbital, followed by intravenous injection of BMSCs with manipulated expression of lncRNA SNHG1, microRNA (miR)-15a, and SMURF1. Subsequent to HGF induction, expression of hepatocyte-related genes, albumin secretion, and glycogen accumulation was increased in BMSCs, suggesting the differentiation of BMSCs into HLCs. Mechanistically, lncRNA SNHG1 bound to miR-15a that targeted SMURF1, and SMURF1 diminished ATG5 and Wnt5a expression by enhancing the ubiquitination of UVRAG. LncRNA SNHG1 or SMURF1 silencing or miR-15a overexpression promoted differentiation of BMSCs into HLCs and repressed cirrhosis of mice by upregulating ATG5 and Wnt5a via UVRAG. Conclusively, lncRNA SNHG1 silencing might facilitate HLC differentiation from mouse BMSCs and alleviate cirrhosis via the miR-15a/SMURF1/UVRAG/ATG5/Wnt5a axis.

Identifiers

PMID35194023
PMCPMC8863836
OpenAlexW4213241964

What OpenQuestion holds

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Registered trials

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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.