Evidence map›Paper›PMID 25120286›Full record

ArticleMediators of inflammation2014

Can the TLR-4-mediated signaling pathway be "a key inflammatory promoter for sporadic TAA"?

Giovanni Ruvolo, Calogera Pisano, Giuseppina Candore, Domenico Lio, Cesira Palmeri, Emiliano Maresi, Carmela R Balistreri

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2014. 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
2.1field-weighted citation impact, top 13% 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, 47 citations in OpenAlex.

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  12. Cyclophilin A contributes to aortopathy induced by postnatal loss of smooth muscle TGFBR1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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  20. Primary biliary cirrhosis is a generalized autoimmune epithelitis.International journal of molecular sciences · 2015
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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

7 authors at 1 institution in 1 country.

Giovanni RuvoloUnit of Cardiac Surgery, Department of Surgery and Oncology, University of Palermo, 90127 Palermo, Italy.
Calogera PisanoUnit of Cardiac Surgery, Department of Surgery and Oncology, University of Palermo, 90127 Palermo, Italy.
Giuseppina CandoreDepartment of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo, Corso Tukory 211, 90134 Palermo, Italy.
Domenico LioDepartment of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo, Corso Tukory 211, 90134 Palermo, Italy.
Cesira PalmeriDepartment of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo, Corso Tukory 211, 90134 Palermo, Italy.
Emiliano MaresiDepartment of Pathologic Anatomy, University of Palermo, 90127 Palermo, Italy.
Carmela R BalistreriDepartment of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo, Corso Tukory 211, 90134 Palermo, Italy.
University of Palermo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thoracic aorta shows with advancing age various changes and a progressive deterioration in structure and function. As a result, vascular remodeling (VR) and medial degeneration (MD) occur as pathological entities responsible principally for the sporadic TAA onset. Little is known about their genetic, molecular, and cellular mechanisms. Recent evidence is proposing the strong role of a chronic immune/inflammatory process in their evocation and progression. Thus, we evaluated the potential role of Toll like receptor- (TLR-) 4-mediated signaling pathway and its polymorphisms in sporadic TAA. Genetic, immunohistochemical, and biochemical analyses were assessed. Interestingly, the rs4986790 TLR4 polymorphism confers a higher susceptibility for sporadic TAA (OR = 14.4, P = 0.0008) and it represents, together with rs1799752 ACE, rs3918242 MMP-9, and rs2285053 MMP-2 SNPs, an independent sporadic TAA risk factor. In consistency with these data, a significant association was observed between their combined risk genotype and sporadic TAA. Cases bearing this risk genotype showed higher systemic inflammatory mediator levels, significant inflammatory/immune infiltrate, a typical MD phenotype, lower telomere length, and positive correlations with histopatological abnormalities, hypertension, smoking, and ageing. Thus, TLR4 pathway should seem to have a key role in sporadic TAA. It might represent a potential useful tool for preventing and monitoring sporadic TAA and developing personalized treatments.

Indexed as

AgedAorta, ThoracicAortic DiseasesFemaleGenetic Predisposition to DiseaseGenotypeHumansImmunohistochemistryMaleMatrix Metalloproteinase 2Middle AgedPolymorphism, GeneticPolymorphism, Single NucleotideSignal TransductionToll-Like Receptor 4Matrix Metalloproteinase 2Toll-Like Receptor 4

Identifiers

PMID25120286
PMCPMC4120489
OpenAlexW2029171570

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.