Evidence map›Paper›PMID 30635025›Full record

ArticleStem cell research & therapy2019

Follistatin-like 1 protects mesenchymal stem cells from hypoxic damage and enhances their therapeutic efficacy in a mouse myocardial infarction model.

Han Shen, Guanghao Cui, Yanqiong Li, Wenxue Ye, Yimin Sun, Zihan Zhang, Jingjing Li, Guiying Xu, Xiansheng Zeng, Yanxia Zhang and 4 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  11. Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Han ShenInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Guanghao CuiInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Yanqiong LiInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Wenxue YeDepartment of Cardiovascular Surgery of the First Affiliated Hospital and Institute for Cardiovascular Science, Soochow University, Suzhou, 215006, China.
Yimin SunInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Zihan ZhangInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Jingjing LiInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Guiying XuInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Xiansheng ZengDepartment of Cardiology of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Yanxia ZhangInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China.
Wencheng ZhangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital of Shandong University, Jinan, China.
Zan HuangJiangsu Province Key Laboratory of Gastrointestinal Nutrition and Animal Health, College of Animal Science and Technology, Nanjing Agriculture University, Nanjing, 210000, China.
Weiqian ChenInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China. chenweiqian@suda.edu.cn.ORCID 0000-0002-9232-9027
Zhenya ShenInstitute for Cardiovascular Science and Department of Cardiovascular Surgery of the First Affiliated Hospital, Soochow University, Suzhou, 215006, China. uuzyshen@aliyun.com.
Soochow University · CNNanjing Agricultural University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCell therapy remains the most promising approach against ischemic heart injury. However, poor survival of engrafted cells in ischemic sites diminishes its therapeutic efficacy. Follistatin-like 1 (Fstl1) is documented as a novel pro-survival cardiokine for cardiomyocytes, and it is protective during ischemic heart injury. In the present study, we characterize the potential of Fstl1 as an effective strategy to enhance hypoxia resistance of donor cells and optimize stem cell-based therapy.

methodsMurine bone marrow-derived mesenchymal stem cells (MSCs) were expanded in monolayer culture and characterized by flow cytometry. MSCs were subjected to hypoxia to mimic cardiac ischemic environment. Expression of Fstl1 was monitored 0, 24, and 48 h following hypoxia. Constitutive expression of Fstl1 in MSCs was achieved by lentivirus-mediated Fstl1 overexpression. Genetically modified MSCs were further collected for cell death and proliferation assay following 48 h of hypoxic treatment. Acute myocardial infarction (MI) model was created by ligating the left anterior descending coronary artery, while control MSCs (MSCs-mCherry) or Fstl1-overexpressing MSCs (MSCs-Fstl1) were injected into the peri-infarct zone simultaneously. Subsequently, retention of the donor cells was evaluated on post-therapy 1, 3, & 7 days. Finally, myocardial function, infarct size, inflammation, and neovascularization of the infarcted hearts were calculated thereafter.

resultsExpression of Fstl1 in hypoxic MSCs declines dramatically in a time-dependent manner. In vitro study further demonstrated that Fstl1 promotes survival and proliferation of hypoxic MSCs. Moreover, Fstl1 significantly prolongs MSC survival/retention after implantation. Finally, transplantation with Fstl1-overexpressing MSCs significantly improves post-MI cardiac function by limiting scar formation, reducing inflammatory response, and enhancing neovascularization.

conclusionsOur results suggest Fstl1 is an intrinsic cardiokine promoting survival and proliferation of MSCs, thereby optimizing their engraftment and therapeutic efficacy during cell therapy.

Indexed as

Mesenchymal Stem Cell TransplantationAnimalsApoptosisCell HypoxiaCell ProliferationCell SurvivalDisease Models, AnimalFollistatin-Related ProteinsHumansLentivirusMesenchymal Stem CellsMiceMyocardial InfarctionMyocardiumMyocytes, CardiacNeovascularization, PhysiologicFollistatin-Related ProteinsFstl1 protein, mouseFollistatin-like 1Mesenchymal stem cellsMyocardial infarctionSurvivalTransplantation

Identifiers

PMID30635025
PMCPMC6330478
OpenAlexW2910572922

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.