Evidence map›Paper›PMID 37920508›Full record

ArticleHeliyon2023

BMSCs alleviate liver cirrhosis by regulating Fstl1/Wnt/β-Catenin signaling pathway.

Hanjing Zhangdi, Xinyu Geng, Ning Li, Ruiling Xu, Ying Hu, Jingyang Liu, Xu Zhang, Jihan Qi, Yingying Tian, Jiawei Qiu and 3 more

Abstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
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

13 authors.

Hanjing ZhangdiDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Xinyu GengDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Ning LiDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Ruiling XuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Ying HuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Jingyang LiuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Xu ZhangDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Jihan QiDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Yingying TianDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Jiawei QiuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Shiling HuangDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Xueyu CangDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Shizhu JinDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Researchers have shown that bone mesenchymal stem cells (BMSCs) can alleviate the progression of liver cirrhosis; however, it is unclear how exactly BMSCs function to cure liver disease. In this study, we used bioinformatics methods to assess differentially expressed genes (DEGs) in liver cirrhosis and found a significantly upregulated gene, Fstl1, in liver cirrhosis. In vivo and in vitro experiments showed that compared with those in the disease model group, the mRNA, and protein expression levels of Fstl1 were significantly reduced after BMSCs treatment, and the β-Catenin protein level was also significantly reduced after BMSCs treatment. Subsequently, we downregulated Fstl1 in activated hepatic stellate cells (HSCs) and found that Wnt and β-Catenin protein expression levels also decreased. Finally, we found that in BMSCs-treated activated HSCs, overexpression of Fstl1 reversed the inhibitory effect of BMSCs on the Wnt/β-Catenin signaling pathway to a certain extent. In summary, our results show that BMSCs can inhibit Wnt/β-Catenin signaling pathway activation by downregulating the protein expression level of Fstl1, thus alleviating cirrhosis. Therefore, targeted regulation of Fstl1 may provide a new therapeutic strategy for the progression of liver cirrhosis.

Indexed as

BMSCsFstl1Liver cirrhosisWnt/β-Catenin

Identifiers

PMID37920508
PMCPMC10618771

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.