Evidence map›Paper›PMID 29353218›Full record

ArticleRedox biology2018

Sulforaphane prevents angiotensin II-induced cardiomyopathy by activation of Nrf2 via stimulating the Akt/GSK-3ß/Fyn pathway.

Ying Xin, Yang Bai, Xin Jiang, Shanshan Zhou, Yuehui Wang, Kupper A Wintergerst, Taixing Cui, Honglei Ji, Yi Tan, Lu Cai

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 176 citations in OpenAlex.

  1. Individual and Combined Cardioprotective Effects of 1,25(OH)Journal of biochemical and molecular toxicology · 2026
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  7. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  8. Review
  9. Sulforaphane and ophthalmic diseases.Food science & nutrition · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Sulforaphane attenuates irradiation induced testis injury in mice.Redox report : communications in free radical research · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

23 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

10 authors at 6 institutions in 2 countries.

Ying XinKey Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun 130021, China; Chinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences at the Wenzhou Medical University, Wenzhou 325035, China; Pediatrics Research Institute, the Department of Pediatrics of the University of Louisville, Louisville 40202, USA.
Yang BaiPediatrics Research Institute, the Department of Pediatrics of the University of Louisville, Louisville 40202, USA; First Hospital of Jilin University, Changchun 130021, China.
Xin JiangPediatrics Research Institute, the Department of Pediatrics of the University of Louisville, Louisville 40202, USA; First Hospital of Jilin University, Changchun 130021, China.
Shanshan ZhouPediatrics Research Institute, the Department of Pediatrics of the University of Louisville, Louisville 40202, USA; First Hospital of Jilin University, Changchun 130021, China.
Yuehui WangFirst Hospital of Jilin University, Changchun 130021, China.
Kupper A WintergerstDivision of Endocrinology of Department of Pediatrics, University of Louisville School of Medicine, Norton Children's Hospital, Louisville 40202, USA; Wendy L. Novak Diabetes Care Center at the University of Louisville, Louisville 40202, USA.
Taixing CuiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia 29208, USA.
Honglei JiFirst Hospital of Jilin University, Changchun 130021, China. Electronic address: jihonglei@aliyun.com.
Yi TanChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences at the Wenzhou Medical University, Wenzhou 325035, China; Pediatrics Research Institute, the Department of Pediatrics of the University of Louisville, Louisville 40202, USA; Wendy L. Novak Diabetes Care Center at the University of Louisville, Louisville 40202, USA. Electronic address: yi.tan@louisville.edu.
Lu CaiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences at the Wenzhou Medical University, Wenzhou 325035, China; Pediatrics Research Institute, the Department of Pediatrics of the University of Louisville, Louisville 40202, USA; Wendy L. Novak Diabetes Care Center at the University of Louisville, Louisville 40202, USA; Department of Pharmacology and Toxicology, the University of Louisville, Louisville 40202, USA.
University of Louisville · USDiabetes Care Center · USJilin University · CNFirst Hospital of Jilin University · CNKosair Children's Hospital · USUniversity of South Carolina · US

Funding

Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
NCCIH NIH HHS P01 AT003961
6 · The paper itself

Abstract

aimsActivation of nuclear factor erythroid 2-related factor 2 (Nrf2) by sulforaphane (SFN) protects from, and deletion of the Nrf2 gene exaggerates, diabetic cardiomyopathy. Angiotensin II (Ang II) plays a critical role in the development of diabetic cardiomyopathy. Therefore, whether SFN prevents Ang II-induced cardiomyopathy through activation of Nrf2 was examined using wild-type, global deletion of Nrf2 gene (Nrf2-KO) and cardiomyocyte-specific overexpression of Nrf2 gene (Nrf2-TG) mice. METHODS AND

resultsAdministration of a subpressor dose of Ang II to wild-type mice induced cardiac oxidative stress, inflammation, remodeling and dysfunction, all of which could be prevented by SFN treatment with Nrf2 up-regulation and activation. Nrf2-KO mice are susceptible, and Nrf2-TG mice are resistant, respectively, to Ang II-induced cardiomyopathy. Meanwhile, the ability of SFN to protect against Ang II-induced cardiac damage was lost in Nrf2-KO mice. Up-regulation and activation of Nrf2 by SFN is accompanied by activation of Akt, inhibition of glycogen synthase kinase (GSK)-3β, and accumulation of Fyn in nuclei. In vitro up-regulation of Nrf2 by SFN was abolished and nuclear Fyn accumulation was increased when cardiac cells were exposed to a PI3K inhibitor or GSK-3β-specific activator.

conclusionThese results suggest that Nrf2 plays a central role in the prevention of Ang II-induced cardiomyopathy, and SFN prevents Ang II-induced cardiomyopathy partially via the Akt/GSK-3β/Fyn-mediated Nrf2 activation.

Indexed as

Angiotensin IIAnimalsDiabetic CardiomyopathiesDisease Models, AnimalGlycogen Synthase Kinase 3 betaHeartHumansIsothiocyanatesMaleMice, KnockoutNF-E2-Related Factor 2Oxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fynSignal TransductionAngiotensin IIFyn protein, mouseGlycogen Synthase Kinase 3 betaIsothiocyanatesNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fynsulforaphaneSulfoxidesAngiotensin IICardiomyopathyNrf2 activatorOxidative stress

Identifiers

PMID29353218
PMCPMC5975128
OpenAlexW2781769970

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.