Evidence map›Paper›PMID 30147446›Full record

ArticleMediators of inflammation2018

TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress.

Veronica Tisato, Stefania Gallo, Elisabetta Melloni, Claudio Celeghini, Angelina Passaro, Giorgio Zauli, Paola Secchiero, Carlo Bergamini, Alessandro Trentini, Gloria Bonaccorsi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 27 citations in OpenAlex.

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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 at 1 institution in 2 countries.

Veronica TisatoDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.ORCID 0000-0001-8448-066X
Stefania GalloDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
Elisabetta MelloniDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
Claudio CeleghiniDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
Angelina PassaroDepartment of Medical Science, University of Ferrara, Ferrara, Italy.
Giorgio ZauliDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.ORCID 0000-0002-3750-8698
Paola SecchieroDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
Carlo BergaminiDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy.
Alessandro TrentiniDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy.ORCID 0000-0003-3579-7921
Gloria BonaccorsiDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
Giuseppe ValacchiDepartment of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy.ORCID 0000-0002-8792-0947
Giovanni ZulianiDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy.
Carlo CervellatiDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy.ORCID 0000-0003-4777-6300
University of Ferrara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objective"Oxinflammation" is a recently coined term that defines the deleterious crosstalk between inflammatory and redox systemic processes, which underlie several diseases. Oxinflammation could be latently responsible for the predisposition of certain healthy individuals to disease development. The oxinflammatory pathway has been recently suggested to play a crucial role in regulating the activity of TNF-related apoptosis-inducing ligand (TRAIL), a TNF superfamily member that can mediate multiple signals in physiological and pathological processes. Therefore, we investigated the associations between TRAIL and key players of vascular redox homeostasis.

methodsWe measured circulating TRAIL levels relative to praoxonas-1, lipoprotein phospholipase-A2, and ceruloplasmin levels in a cohort of healthy subjects (

resultsMultivariate analysis revealed that ceruloplasmin levels were significantly inversely associated with TRAIL levels (

conclusionThe results indicated that in an inflammatory milieu, TRAIL downregulates ceruloplasmin expression, highlighting a signaling axis involving TRAIL and ceruloplasmin that are linked via inflammation and providing important insights with potential clinical implications.

Indexed as

AgedCeruloplasminFemaleHumansInflammationLeukocytes, MononuclearMaleMiddle AgedMultivariate AnalysisOxidative StressSignal TransductionTNF-Related Apoptosis-Inducing LigandCeruloplasminTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID30147446
PMCPMC6083483
OpenAlexW2883531432

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.