Evidence map›Paper›PMID 35165707›Full record

ArticleEuropean heart journal2022

Galectin 3 enhances platelet aggregation and thrombosis via Dectin-1 activation: a translational study.

Yufei Chen, Wanrong Fu, Yunbo Zheng, Jing Yang, Yangyang Liu, Zhiyong Qi, Meiling Wu, Zhichao Fan, Kanhua Yin, Yunfeng Chen and 6 more

Open access · greenAbstract read
In one paragraph

Article in European heart journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

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  10. Colonic Submucosa Targeted Delivery of Probiotic and Rhein for Ulcerative Colitis Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Current and novel biomarkers in cardiogenic shock.European journal of heart failure · 2025
    Review
  12. Article
  13. Observational
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 2 countries.

Yufei ChenAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.ORCID 0000-0002-4346-6391
Wanrong FuCardiovascular Institute of Zhengzhou University, Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0002-7521-5204
Yunbo ZhengCardiovascular Institute of Zhengzhou University, Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jing YangCardiovascular Institute of Zhengzhou University, Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yangyang LiuCardiovascular Institute of Zhengzhou University, Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0001-8296-7095
Zhiyong QiDepartment of Biochemistry and Molecular Biology, NHC Key Laboratory of Glycoconjugates Research, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Meiling WuDepartment of Biochemistry and Molecular Biology, NHC Key Laboratory of Glycoconjugates Research, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0002-2654-4896
Zhichao FanDepartment of Immunology, School of Medicine, UConn Health, Farmington, CT, USA.ORCID 0000-0001-5385-9626
Kanhua YinDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-4769-3129
Yunfeng ChenDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, USA.ORCID 0000-0001-7618-107X
Wen GaoDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-9857-5966
Zhongren DingCardiovascular Institute of Zhengzhou University, Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jianzeng DongCardiovascular Institute of Zhengzhou University, Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0001-7299-7805
Qi LiAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Si ZhangDepartment of Biochemistry and Molecular Biology, NHC Key Laboratory of Glycoconjugates Research, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0002-5682-4995
Liang HuAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.ORCID 0000-0001-5559-3913
First Affiliated Hospital of Zhengzhou University · CNFudan University · CNScripps Research Institute · USShanghai University of Traditional Chinese Medicine · CNHarvard University · USUConn Health · US

Funding

Inhibiting biomechanical platelet aggregation to prevent arterial thrombosis without compromising hemostasisR00HL153678 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI CHEN, YUNFENG · 2022 to 2024
$746k
NHLBI NIH HHS R00 HL153678
6 · The paper itself

Abstract

aimsGalectin-3, a β-galactoside-binding lectin, is abnormally increased in cardiovascular disease. Plasma Galectin-3 receives a Class II recommendation for heart failure management and has been extensively studied for multiple cellular functions. The direct effects of Galectin-3 on platelet activation remain unclear. This study explores the direct effects of Galectin-3 on platelet activation and thrombosis. METHODS AND

resultsA strong positive correlation between plasma Galectin-3 concentration and platelet aggregation or whole blood thrombus formation was observed in patients with coronary artery disease (CAD). Multiple platelet function studies demonstrated that Galectin-3 directly potentiated platelet activation and in vivo thrombosis. Mechanistic studies using the Dectin-1 inhibitor, laminarin, and Dectin-1-/- mice revealed that Galectin-3 bound to and activated Dectin-1, a receptor not previously reported in platelets, to phosphorylate spleen tyrosine kinase and thus increased Ca2+ influx, protein kinase C activation, and reactive oxygen species production to regulate platelet hyperreactivity. TD139, a Galectin-3 inhibitor in a Phase II clinical trial, concentration dependently suppressed Galectin-3-potentiated platelet activation and inhibited occlusive thrombosis without exacerbating haemorrhage in ApoE-/- mice, which spontaneously developed increased plasma Galectin-3 levels. TD139 also suppressed microvascular thrombosis to protect the heart from myocardial ischaemia-reperfusion injury in ApoE-/- mice.

conclusionGalectin-3 is a novel positive regulator of platelet hyperreactivity and thrombus formation in CAD. As TD139 has potent antithrombotic effects without bleeding risk, Galectin-3 inhibitors may have therapeutic advantages as potential antiplatelet drugs for patients with high plasma Galectin-3 levels.

Indexed as

Platelet AggregationThrombosisAnimalsApolipoproteins EBlood PlateletsCalciumDectin-1Fibrinolytic AgentsGalectin 3Lectins, C-TypeMiceMice, Knockout, ApoEPlatelet ActivationPlatelet Aggregation InhibitorsProtein Kinase CReactive Oxygen SpeciesApolipoproteins ECalciumDectin-1Fibrinolytic AgentsGalectin 3Lectins, C-TypePlatelet Aggregation InhibitorsProtein Kinase CReactive Oxygen SpeciesSyk KinaseAntithromboticCardiovascular diseasesDectin-1Galectin-3Platelet hyperreactivityTD139

Identifiers

PMID35165707
PMCPMC9989600
OpenAlexW4207066019

What OpenQuestion holds

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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.