Evidence map›Paper›PMID 37285055›Full record

ArticleApoptosis : an international journal on programmed cell death2023

CHI3L1 promotes myocardial fibrosis via regulating lncRNA TUG1/miR-495-3p/ETS1 axis.

Yunpeng Sun, Xue Shan, Jiantao Guo, Xuguang Liu, Dashi Ma

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. ETS‑1/ETS‑2 transcription factors in CVD (Review).International journal of molecular medicine · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. 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

5 authors at 2 institutions in 1 country.

Yunpeng SunDepartment of Cardiac Surgery, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin, 130021, China.
Xue ShanDepartment of Cardiac Surgery, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin, 130021, China.
Jiantao GuoDepartment of Cardiac Surgery, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin, 130021, China.
Xuguang LiuDepartment of Cardiac Surgery, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin, 130021, China. liuxuguang2022@outlook.com.
Dashi MaDepartment of Cardiac Surgery, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin, 130021, China. mads@jlu.edu.cn.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal levels of CHI3L1 and lnc TUG1 are often associated with myocardial fibrosis, and their specific expressions may be closely related to the process of myocardial fibrosis. In addition, CHI3L1 was found to significantly up-regulate the expression of lncTUG1. Therefore, this study further explored the major role of CHI3L1 in regulating the progression of myocardial fibrosis. Myocardial fibrosis in mice was established using an angiotensin (Ang II) model, and the degree of myocardial fibrosis was assessed by qPCR, western blot and pathological techniques. HL-1 cells with overexpression and silencing of CHI3L1 were constructed, and the cell migration ability was detected using the Transwell method. Biological information was used to predict the potential target miRNA of lnc TUG1, and the interaction between them was verified by dual luciferase reporter assay. Using functional rescue assay and the rAAV9 technique, CHI3L1 was verified to affect the fibrotic process of myocardial cells by regulating the lnc TUG1/miR-495-3p/ETS1 axis in vitro and in vivo. The myocardial fibrosis index in the model group was significantly upregulated, and expression of both CHI3L1 and lnc TUG1 was upregulated. Pathological results revealed fibrosis and collagen deposition in the myocardium. Overexpression of lnc TUG1 reversed the inhibitory effect of CHI3L1 silencing on myocardial fibrosis. Mechanistically, CH3L1 upregulates the expression of lnc TUG1, and lnc TUG1 weakens the inhibition of ETS1 through sponge absorption of miR-495-3p, promoting the process of myocardial fibrosis.

Indexed as

MicroRNAsRNA, Long NoncodingAnimalsApoptosisCell MovementChitinase-3-Like Protein 1MiceMyocardiumSignal TransductionChil1 protein, mouseChitinase-3-Like Protein 1MicroRNAsRNA, Long NoncodingCHI3L1ETS1Lnc TUG1miR-495-3pMyocardial fibrosis

Identifiers

PMID37285055
OpenAlexW4379599591

What OpenQuestion 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 OpenQuestion graph.