Evidence map›Paper›PMID 38829964›Full record

ArticleJournal of medicinal chemistry2024

Glycopolymer Inhibitors of Galectin-3 Suppress the Markers of Tissue Remodeling in Pulmonary Hypertension.

Antonín Sedlář, David Vrbata, Kateřina Pokorná, Kristýna Holzerová, Jakub Červený, Olga Kočková, Markéta Hlaváčková, Martina Doubková, Jana Musílková, Vladimír Křen and 3 more

Abstract read
In one paragraph

Article in Journal of medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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

13 authors.

Antonín SedlářLaboratory of Biomaterials and Tissue Engineering, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
David VrbataLaboratory of Biotransformation, Institute of Microbiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Kateřina PokornáLaboratory of Biomaterials and Tissue Engineering, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Kristýna HolzerováLaboratory of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Jakub ČervenýLaboratory of Biotransformation, Institute of Microbiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Olga KočkováLaboratory of Analytical Chemistry, Institute of Macromolecular Chemistry of the Czech Academy of Sciences, Heyrovského nám. 1888, Prague 6 CZ-162 00, Czech Republic.ORCID 0000-0003-3761-4033
Markéta HlaváčkováLaboratory of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Martina DoubkováLaboratory of Biomaterials and Tissue Engineering, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.ORCID 0000-0002-4955-4093
Jana MusílkováLaboratory of Biomaterials and Tissue Engineering, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Vladimír KřenLaboratory of Biotransformation, Institute of Microbiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.ORCID 0000-0002-1091-4020
František KolářLaboratory of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Lucie BačákováLaboratory of Biomaterials and Tissue Engineering, Institute of Physiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.
Pavla BojarováLaboratory of Biotransformation, Institute of Microbiology of the Czech Academy of Sciences, Vídeňská 1083, Prague 4 CZ-142 00, Czech Republic.ORCID 0000-0001-7069-0973

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension is a cardiovascular disease with a low survival rate. The protein galectin-3 (Gal-3) binding β-galactosides of cellular glycoproteins plays an important role in the onset and development of this disease. Carbohydrate-based drugs that target Gal-3 represent a new therapeutic strategy in the treatment of pulmonary hypertension. Here, we present the synthesis of novel hydrophilic glycopolymer inhibitors of Gal-3 based on a polyoxazoline chain decorated with carbohydrate ligands. Biolayer interferometry revealed a high binding affinity of these glycopolymers to Gal-3 in the subnanomolar range. In the cell cultures of cardiac fibroblasts and pulmonary artery smooth muscle cells, the most potent glycopolymer

Indexed as

Galectin 3Hypertension, PulmonaryAnimalsBiomarkersCells, CulturedFibroblastsHumansMalePolymersPulmonary ArteryRatsTissue DistributionBiomarkersGalectin 3Polymers

Identifiers

PMID38829964
PMCPMC11181325

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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.