Evidence map›Paper›PMID 30725211›Full record

ArticleEuropean journal of nutrition2020

Targeting endothelial-to-mesenchymal transition: the protective role of hydroxytyrosol sulfate metabolite.

Erika Terzuoli, Ginevra Nannelli, Antonio Giachetti, Lucia Morbidelli, Marina Ziche, Sandra Donnini

Abstract read
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In one paragraph

Article in European journal of nutrition, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
1.6field-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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Investigation of the protective effects of hydroxytyrosol on erythrocyte deformability during hind limb ischemia-reperfusion injury in rats.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2026
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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

6 authors at 1 institution in 1 country.

Erika TerzuoliDepartment of Life Sciences, University of Siena, Siena, Italy.ORCID http://orcid.org/0000-0001-9248-4505
Ginevra NannelliDepartment of Life Sciences, University of Siena, Siena, Italy.ORCID http://orcid.org/0000-0002-7856-9622
Antonio GiachettiDepartment of Life Sciences, University of Siena, Siena, Italy.
Lucia MorbidelliDepartment of Life Sciences, University of Siena, Siena, Italy.ORCID http://orcid.org/0000-0001-8148-7049
Marina ZicheDepartment of Life Sciences, University of Siena, Siena, Italy. marina.ziche@unisi.it.ORCID http://orcid.org/0000-0002-9564-214X
Sandra DonniniDepartment of Life Sciences, University of Siena, Siena, Italy. sandra.donnini@unisi.it.ORCID http://orcid.org/0000-0001-6617-1644
University of Siena · IT

Funding

Progetti di Rilevante Interesse Nazionale 20152HKF3Z
6 · The paper itself

Abstract

purposeEndothelial-to-mesenchymal transition (EndMT) plays an important role in pathogenesis of a number of inflammatory diseases. Hydroxytyrosol (HT) and, particularly, its major plasma metabolite HT-3O sulfate (HT-3Os) are known olive oil antioxidant and anti-inflammatory polyphenols which exert benefits against vascular diseases by improving endothelial function. However, to date the HT-3Os role in EndMT is not well known.

methodsTo investigate the HT-3Os effects on EndMT in the inflamed endothelium, we used an in vitro model of endothelial dysfunction, challenging endothelial cells (EC), human umbilical EC (HUVEC) and human retinal EC (HREC) with Interleukin-1β (IL-1β), an inflammatory agent. HREC were used as a specific model to investigate HT-3Os effects on vascular retinal diseases.

resultsWe found that IL-1β treatment-induced EndMT phenotype in both cell models, also changing cell morphology. HT-3Os protected EC against IL-1β effects, recovering cell morphology and phenotype. Mechanistically, HT-3Os targeting fibroblast growth factor receptor 1 FGFR1 expression and let-7 miRNA, controlled transforming growth factor beta (TGF-β) signalling in EC, downregulating transcription factors expression (SNAI1 and ZEB2) and gene expression of late EndMT markers (FN1, VIM, NOTCH3, CNN1, MMP2 and MMP9).

conclusionThese results demonstrate that HT-3Os blunts pathological EndMT in inflamed EC, maintaining high let-7 miRNA expression and preventing activation of TGF-β signalling.

Indexed as

Anti-Inflammatory AgentsAntioxidantsCells, CulturedEndotheliumInflammationIn Vitro TechniquesMesodermPhenylethyl AlcoholSulfates3,4-dihydroxyphenylethanolAnti-Inflammatory AgentsAntioxidantsPhenylethyl AlcoholSulfatesEndothelial cellsEndothelial mesenchymal transitionFGFR1Hydroxytyrosol-3O sulfateLet-7TGF-β

Identifiers

PMID30725211
OpenAlexW2911785505

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.