Evidence map›Paper›PMID 42737642›Full record

ArticleInternational journal of molecular sciences2026

Endocan Participates in TGF-β/Smad and AKT/ERK Signaling Coordination and lncRNA Modulation in Human Cardiac Fibroblasts.

Federica Aliquò, Alice Pantano, Giulia Giuffrè, Davide Labellarte, Angela Avenoso, Adele Campo, Giovanna Vermiglio, Giuseppe M Campo, Angela D'Ascola, Michele Scuruchi

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In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Federica AliquòDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.
Alice PantanoDepartment of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.
Giulia GiuffrèDepartment of Mathematical and Computer Sciences, Physical Sciences and Earth Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres 31, 98166 Messina, Italy.
Davide LabellarteDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres 31, 98166 Messina, Italy.
Angela AvenosoDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.
Adele CampoDepartment of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.ORCID 0000-0002-2664-7457
Giovanna VermiglioDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.ORCID 0000-0003-3226-8522
Giuseppe M CampoDepartment of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.
Angela D'AscolaDepartment of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.ORCID 0000-0001-7530-1316
Michele ScuruchiDepartment of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.ORCID 0000-0002-5282-1690

Funding

University of Messina FFABR_2023
6 · The paper itself

Abstract

Endocan, a soluble dermatan sulfate proteoglycan, is increasingly recognized as a regulator of key cellular pathways in both physiological and pathological contexts. While TGF-β is a central mediator of fibrotic remodeling, the role of endocan in this process remains elusive. By performing a transcriptomic dataset analysis [GSE116250], we found that endocan expression is upregulated and correlates with fibrotic markers in human failing hearts. We investigated the role of endocan in an in vitro model of cardiac fibroblasts stimulated with TGF-β. Our results identified endocan as a TGF-β-responsive gene in primary human cardiac fibroblasts. Indeed, by inhibiting endocan expression using a specific siRNA, we demonstrated that this proteoglycan is required for the full expression of key fibrosis-related genes (Col1a1, α-SMA, MMP-3, and MMP-9) and modulates the expression of long non-coding RNAs (MALAT1, H19 and HOTAIR), which are essential for the epigenetic control of the fibroblast phenotype. These effects depend on the modulation of both canonical (SMAD3) and non-canonical (AKT and ERK1/2) TGF-β pathways. Taken together, these findings indicate that endocan is required for the coordinated activation of canonical and non-canonical TGF-β signaling during fibroblast transdifferentiation and suggest its potential involvement in the molecular mechanisms underlying cardiac fibrosis.

Indexed as

FibroblastsMAP Kinase Signaling SystemMyocardiumNeoplasm ProteinsProteoglycansProto-Oncogene Proteins c-aktRNA, Long NoncodingSmad ProteinsTransforming Growth Factor betaCells, CulturedFibrosisGene Expression RegulationHumansSignal TransductionESM1 protein, humanNeoplasm ProteinsProteoglycansProto-Oncogene Proteins c-aktRNA, Long NoncodingSmad ProteinsTransforming Growth Factor betacardiac fibrosisendocan (ESM-1)lncRNAsmyofibroblast transdifferentiationproteoglycansTGF-β signaling coordination

Identifiers

PMID42737642
PMCPMC13566329

What Socratic holds

Textmetadata
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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 Socratic graph.