Evidence map›Paper›PMID 28455954›Full record

ArticleOncotarget2017

Galectin-1 expression imprints a neurovascular phenotype in proliferative retinopathies and delineates responses to anti-VEGF.

Magali E Ridano, Paula V Subirada, María C Paz, Valeria E Lorenc, Juan C Stupirski, Ana L Gramajo, José D Luna, Diego O Croci, Gabriel A Rabinovich, María C Sánchez

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Stromal-Like Cells and Retinal Pigment Epithelium Modulate Choroidal Sprouting Through Galectin-1-Dependent and Independent Pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  7. Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023
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  17. Activated αScientific reports · 2019
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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 7 institutions in 2 countries.

Magali E RidanoCentro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
Paula V SubiradaCentro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
María C PazCentro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
Valeria E LorencCentro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
Juan C StupirskiLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina.
Ana L GramajoCentro Privado de Ojos Romagosa-Fundación VER, Córdoba, Argentina.
José D LunaCentro Privado de Ojos Romagosa-Fundación VER, Córdoba, Argentina.
Diego O CrociLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina.
Gabriel A RabinovichLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), CONICET, Buenos Aires, Argentina.
María C SánchezCentro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
Universidad Nacional de Córdoba · ARHospital Privado · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARExperimental Medicine and Biology Institute · ARInstituto de Histología y Embriología de Mendoza · ARJohns Hopkins Medicine · USUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neovascular retinopathies are leading causes of irreversible blindness. Although vascular endothelial growth factor (VEGF) inhibitors have been established as the mainstay of current treatment, clinical management of these diseases is still limited. As retinal impairment involves abnormal neovascularization and neuronal degeneration, we evaluated here the involvement of galectin-1 in vascular and non-vascular alterations associated with retinopathies, using the oxygen-induced retinopathy (OIR) model. Postnatal day 17 OIR mouse retinas showed the highest neovascular profile and exhibited neuro-glial injury as well as retinal functional loss, which persisted until P26 OIR. Concomitant to VEGF up-regulation, galectin-1 was highly expressed in P17 OIR retinas and it was mainly localized in neovascular tufts. In addition, OIR induced remodelling of cell surface glycophenotype leading to exposure of galectin-1-specific glycan epitopes. Whereas VEGF returned to baseline levels at P26, increased galectin-1 expression persisted until this time period. Remarkably, although anti-VEGF treatment in P17 OIR improved retinal vascularization, neither galectin-1 expression nor non-vascular and functional alterations were attenuated. However, this functional defect was partially prevented in galectin-1-deficient (Lgals1-/-) OIR mice, suggesting the importance of targeting both VEGF and galectin-1 as non-redundant independent pathways. Supporting the clinical relevance of these findings, we found increased levels of galectin-1 in aqueous humor from patients with proliferative diabetic retinopathy and neovascular glaucoma. Thus, using an OIR model and human samples, we identified a role for galectin-1 accompanying vascular and non-vascular retinal alterations in neovascular retinopathies.

Indexed as

AnimalsDisease Models, AnimalGalectin 1HumansMicePhenotypeRetinitis PigmentosaVascular Endothelial Growth Factor AGalectin 1Vascular Endothelial Growth Factor Agalectin-1neovascularizationneurodegenerationretinopathiesvascular endothelial growth factor

Identifiers

PMID28455954
PMCPMC5464805
OpenAlexW2606781244

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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.