Evidence map›Paper›PMID 39114443›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2024

The molecular mechanism responsible for HbSC retinopathy may depend on the action of the angiogenesis-related genes

Sueli Matilde da Silva Costa, Mirta Tomie Ito, Pedro Rodrigues Sousa da Cruz, Bruno Batista De Souza, Vinicius Mandolesi Rios, Victor de Haidar E Bertozzo, Ana Carolina Lima Camargo, Marina Gonçalves Monteiro Viturino, Carolina Lanaro, Dulcinéia Martins de Albuquerque and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2024. 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

16 authors.

Sueli Matilde da Silva CostaCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Mirta Tomie ItoCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Pedro Rodrigues Sousa da CruzCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Bruno Batista De SouzaCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Vinicius Mandolesi RiosCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Victor de Haidar E BertozzoCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Ana Carolina Lima CamargoCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Marina Gonçalves Monteiro ViturinoCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.
Carolina LanaroCentro de Hematologia e Hemoterapia, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Dulcinéia Martins de AlbuquerqueCentro de Hematologia e Hemoterapia, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Amanda Morato do CantoDepartamento de Medicina Translacional, Faculdade de Ciências Médicas, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Sara Teresinha Olalla SaadCentro de Hematologia e Hemoterapia, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Stephanie Ospina-PrietoCentro de Hematologia e Hemoterapia, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Margareth Castro OzeloCentro de Hematologia e Hemoterapia, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Fernando Ferreira CostaCentro de Hematologia e Hemoterapia, Universidade Estadual de Campinas-UNICAMP, Campinas, Brazil.
Mônica Barbosa de MeloCenter for Molecular Biology and Genetic Engineering, State University of Campinas-UNICAMP, Campinas, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HbSC disease, a less severe form of sickle cell disease, affects the retina more frequently and patients have higher rates of proliferative retinopathy that can progress to vision loss. This study aimed to identify differences in the expression of endothelial cell-derived molecules associated with the pathophysiology of proliferative sickle cell retinopathy (PSCR). RNAseq was used to compare the gene expression profile of circulating endothelial colony-forming cells from patients with SC hemoglobinopathy and proliferative retinopathy (n = 5), versus SC patients without retinopathy (n = 3). Real-time polymerase chain reaction (qRT-PCR) was used to validate the RNAseq results. A total of 134 differentially expressed genes (DEGs) were found. DEGs were mainly associated with vasodilatation, type I interferon signaling, innate immunity and angiogenesis. Among the DEGs identified, we highlight the most up-regulated genes

Indexed as

Nerve Tissue ProteinsReceptors, ImmunologicRetinal NeovascularizationRoundabout ProteinsAdultAngiogenesisEndothelial CellsFemaleHumansMaleNerve Tissue ProteinsReceptors, ImmunologicRoundabout Proteinsangiogenesisdifferentially expressed genesendothelial colony forming cellsproliferative sickle cell retinopathytranscriptome

Identifiers

PMID39114443
PMCPMC11303203

What OpenQuestion holds

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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.