Evidence map›Paper›PMID 33816481›Full record

ArticleFrontiers in cell and developmental biology2021

Inhibition of TGF-β/Smad3 Signaling Disrupts Cardiomyocyte Cell Cycle Progression and Epithelial-Mesenchymal Transition-Like Response During Ventricle Regeneration.

Yuanyuan Peng, Wenyuan Wang, Yunzheng Fang, Haichen Hu, Nannan Chang, Meijun Pang, Ye-Fan Hu, Xueyu Li, Han Long, Jing-Wei Xiong and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Review
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  8. Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Optogenetic control of YAP can enhance the rate of wound healing.Cellular & molecular biology letters · 2023
    Article
  13. Review
  14. Review
  15. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Yuanyuan PengSchool of Life Sciences, Fudan University, Shanghai, China.
Wenyuan WangSchool of Life Sciences, Fudan University, Shanghai, China.
Yunzheng FangSchool of Life Sciences, Fudan University, Shanghai, China.
Haichen HuShanghai Medical College, Fudan University, Shanghai, China.
Nannan ChangInstitute of Molecular Medicine, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing, China.
Meijun PangInstitute of Molecular Medicine, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing, China.
Ye-Fan HuSchool of Life Sciences, Fudan University, Shanghai, China.
Xueyu LiSchool of Life Sciences, Fudan University, Shanghai, China.
Han LongSchool of Life Sciences, Fudan University, Shanghai, China.
Jing-Wei XiongInstitute of Molecular Medicine, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing, China.
Ruilin ZhangSchool of Basic Medical Sciences, Wuhan University, Wuhan, China.
Fudan University · CNPeking University · CNShanghai Medical College of Fudan University · CNUniversity of Hong Kong · HKWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unlike mammals, zebrafish can regenerate injured hearts even in the adult stage. Cardiac regeneration requires the coordination of cardiomyocyte (CM) proliferation and migration. The TGF-β/Smad3 signaling pathway has been implicated in cardiac regeneration, but the molecular mechanisms by which this pathway regulates CM proliferation and migration have not been fully illustrated. Here, we investigated the function of TGF-β/Smad3 signaling in a zebrafish model of ventricular ablation. Multiple components of this pathway were upregulated/activated after injury. Utilizing a specific inhibitor of Smad3, we detected an increased ratio of unrecovered hearts. Transcriptomic analysis suggested that the TGF-β/Smad3 signaling pathway could affect CM proliferation and migration. Further analysis demonstrated that the CM cell cycle was disrupted and the epithelial-mesenchymal transition (EMT)-like response was impaired, which limited cardiac regeneration. Altogether, our study reveals an important function of TGF-β/Smad3 signaling in CM cell cycle progression and EMT process during zebrafish ventricle regeneration.

Indexed as

cell cycleEMT-like responseSmad3TGF-βventricle regeneration

Identifiers

PMID33816481
PMCPMC8010688
OpenAlexW3137715963

What OpenQuestion holds

Textmetadata
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.