Evidence map›Paper›PMID 25787015›Full record

ArticleScientific reports2015

bFGF regulates autophagy and ubiquitinated protein accumulation induced by myocardial ischemia/reperfusion via the activation of the PI3K/Akt/mTOR pathway.

Zhou-Guang Wang, Yue Wang, Yan Huang, Qin Lu, Lei Zheng, Dong Hu, Wen-Ke Feng, Yan-Long Liu, Kang-Ting Ji, Hong-Yu Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
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  5. The mMolecular and cellular biochemistry · 2024
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  6. Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023
    Review
  7. Article
  8. Cirsilineol Treatment Attenuates PMInternational journal of molecular sciences · 2022
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  9. Article
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  11. Review
  12. Therapeutic mechanism ofFrontiers in pharmacology · 2022
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  16. Review
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  18. Article
  19. Review
  20. Article

4 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 1 country.

Zhou-Guang Wang1] School of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China [2] Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Jilin University, Changchun, 130012, China.
Yue Wang1] School of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China [2] Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Jilin University, Changchun, 130012, China.
Yan HuangSchool of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China.
Qin LuDepartment of Pediatric Cardiology, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, China.
Lei ZhengDepartment of Ultrasound, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, China.
Dong HuDepartment of Medical Immunology, Medical School, Anhui University of Science and Technology, Huainan 232001, China.
Wen-Ke FengSchool of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China.
Yan-Long LiuSchool of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China.
Kang-Ting JiDepartment of Pediatric Cardiology, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, China.
Hong-Yu ZhangSchool of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China.
Xiao-Bing FuInstitute of Basic Medical Science, Chinese PLA General Hospital, Beijing 100853, China.
Xiao-Kun Li1] School of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China [2] Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Jilin University, Changchun, 130012, China.
Mao-Ping ChuDepartment of Pediatric Cardiology, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, China.
Jian XiaoSchool of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China.
Wenzhou Medical University · CNAnhui University of Science and Technology · CNChinese PLA General Hospital · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is involved in the development and/or progression of many diseases, including myocardial ischemia/reperfusion (I/R). In this study, we hypothesized a protective role of basic fibroblast growth factor (bFGF) both in vivo and in vitro and demonstrated that excessive autophagy and ubiquitinated protein accumulation is involved in the myocardial I/R model. Our results showed that bFGF improved heart function recovery and increased the survival of cardiomyocytes in myocardial I/R model. The protective effect of bFGF is related to the inhibition of LC3II levels. Additionally, bFGF enhances the clearance of Ub by p62 and increases the survival of H9C2 cells. Moreover, silencing of p62 partially blocks the clearance of Ub and abolishes the anti-apoptosis effect of bFGF. An shRNA against the autophagic machinery Atg7 increased the survival of H9C2 cells co-treated with bFGF and rapamycin. bFGF activates the downstream signaling of the PI3K/Akt/mTOR pathway. These results indicate that the role of bFGF in myocardial I/R recovery is related to the inhibition of excessive autophagy and increased ubiquitinated protein clearance via the activation of PI3K/Akt/mTOR signaling. Overall, our study suggests a new direction for bFGF drug development for heart disease and identifies protein signaling pathways involved in bFGF action.

Indexed as

Signal TransductionAnimalsApoptosisCell LineDisease Models, AnimalEchocardiographyFibroblast Growth Factor 2FibrosisGene SilencingHumansMaleMiceMyocardial Reperfusion InjuryMyocytes, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktFibroblast Growth Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesUbiquitinated Proteins

Identifiers

PMID25787015
PMCPMC4365411
OpenAlexW1998055848

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.