Evidence map›Paper›PMID 42398184›Full record

ArticleEBioMedicine2026

P2Y12-P-selectin-mediated platelet activation in a murine model of dengue-associated thrombocytopenia.

Viviane Lima Batista, Jenniffer Ramos Martins, Angélica Samer Lallo Dias, Talita Cristina Martins Fonseca, Letícia Soldati Silva, Felipe Emanuel Oliveira Rocha, Pedro Augusto Carvalho Costa, Wallison Nunes Silva, Jessica Aparecida Barsalini Pereira, Arielle Teixeira Silva and 10 more

Abstract read
In one paragraph

Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

20 authors.

Viviane Lima BatistaDepartment of Microbiology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Jenniffer Ramos MartinsDepartment of Biochemistry and Immunology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Angélica Samer Lallo DiasDepartment of Biochemistry and Immunology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Talita Cristina Martins FonsecaDepartment of Biochemistry and Immunology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Letícia Soldati SilvaDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Felipe Emanuel Oliveira RochaDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Pedro Augusto Carvalho CostaDepartment of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Wallison Nunes SilvaDepartment of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Jessica Aparecida Barsalini PereiraDepartment of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Arielle Teixeira SilvaDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Maria Luiza CanalisDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Maisa AntunesDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Pedro Pires Goulart GuimarãesDepartment of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Gustavo Batista MenezesDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Adriano de Paula SabinoLaboratory of Clinical, Experimental and Molecular Haematology, Department of Clinical and Toxicological Analysis Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Lirlândia Pires SousaDepartment of Clinical and Toxicological Analysis, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Celso Martins Queiroz-JuniorDepartment of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Eugenio Damaceno HottzLaboratory of Immunothrombosis, Department of Biochemistry, Universidade Federal de Juiz de Fora, Juiz de Fora, Brazil.
Mauro Martins TeixeiraDepartment of Biochemistry and Immunology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Vivian Vasconcelos CostaDepartment of Microbiology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; Department of Morphology; Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Electronic address: vivianvcosta@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDengue virus (DENV) infection frequently leads to thrombocytopenia, a hallmark of severe disease. However, the underlying mechanisms remain incompletely defined. Therefore, this study aimed to investigate the mechanisms underlying dengue-associated thrombocytopenia in a murine model, with a focus on defective thrombopoiesis and platelet activation.

methodsUsing a murine model that recapitulates key haematological and inflammatory features of human dengue, we investigated the impact of DENV infection on megakaryopoiesis, platelet activation, and thromboinflammatory responses. Bone marrow cellularity, megakaryocyte integrity, circulating cytokines and chemokines, platelet activation markers, and vascular injury were assessed. Pharmacological inhibition of P-selectin and blockade of the P2Y12 receptor with clopidogrel were used to evaluate the contribution of platelet activation pathways.

findingsDENV infection impaired megakaryopoiesis, inducing necrotic loss of bone marrow megakaryocytes and leukocytes as early as day 3 post-infection, accompanied by bone marrow aplasia and a compensatory increase in thrombopoietin levels. Systemically, infection triggered P-selectin-dependent platelet activation and platelet-leucocyte aggregate formation, alongside elevated circulating chemokines (CXCL4, CCL5, and CXCL1), vascular leakage in the liver and lungs, and fibrin deposition in pulmonary tissue, consistent with enhanced thromboinflammation. Pharmacological blockade of P-selectin or inhibition of P2Y12 signalling restored platelet counts, preserved megakaryocyte numbers, and attenuated systemic inflammatory responses.

interpretationThese findings indicate that DENV-induced thrombocytopenia arises from the combined effects of impaired megakaryopoiesis and platelet hyperactivation, highlighting platelet activation pathways as potential therapeutic targets for dengue-associated thromboinflammatory complications.

fundingThis work was supported by CNPq, FAPEMIG, Instituto Serrapilheira, and the ASH Global Research Award (465425/2014-3; 408527/2024-2; 163937/2022-2; 25036/2014-3; RED-00202-22 29568-1; APQ-04650-23 and APQ-02618 23).

Indexed as

DenguePlatelet ActivationP-SelectinReceptors, Purinergic P2Y12ThrombocytopeniaAnimalsBlood PlateletsChemokinesCytokinesDengue VirusDisease Models, AnimalHumansMaleMegakaryocytesMiceSignal TransductionChemokinesCytokinesP-SelectinReceptors, Purinergic P2Y12Dengue virusMegakaryopoiesisPlatelet activationP-SelectinThrombocytopeniaThromboinflammation

Identifiers

PMID42398184
PMCPMC13351385

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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.