Evidence map›Paper›PMID 29849898›Full record

ArticleOxidative medicine and cellular longevity2018

From Oxidative Stress Damage to Pathways, Networks, and Autophagy via MicroRNAs.

Nikolai Engedal, Eva Žerovnik, Alexander Rudov, Francesco Galli, Fabiola Olivieri, Antonio Domenico Procopio, Maria Rita Rippo, Vladia Monsurrò, Michele Betti, Maria Cristina Albertini

Abstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
–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

50 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

10 authors.

Nikolai EngedalNordic EMBL Partnership for Molecular Medicine, Centre for Molecular Medicine Norway (NCMM), University of Oslo, P.O. Box 1137, Blindern, 0318 Oslo, Norway.ORCID 0000-0003-3718-3464
Eva ŽerovnikDepartment of Biochemistry and Molecular and Structural Biology, Jožef Stefan Institute and Center of Excellence for Integrated Approaches in Chemistry and Biology of Proteins (CipKeBip), Ljubljana, Slovenia.ORCID 0000-0002-9793-8200
Alexander RudovDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy.
Francesco GalliLaboratory of Clinical Biochemistry and Nutrition, Department of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.
Fabiola OlivieriDepartment of Molecular and Clinical Sciences, Marche Polytechnic University, Ancona, Italy.
Antonio Domenico ProcopioDepartment of Molecular and Clinical Sciences, Marche Polytechnic University, Ancona, Italy.
Maria Rita RippoDepartment of Molecular and Clinical Sciences, Marche Polytechnic University, Ancona, Italy.ORCID 0000-0003-3024-3495
Vladia MonsurròDepartment of Medicine, University of Verona, Verona, Italy.
Michele BettiDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy.
Maria Cristina AlbertiniDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy.ORCID 0000-0003-4549-1475

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress can alter the expression level of many microRNAs (miRNAs), but how these changes are integrated and related to oxidative stress responses is poorly understood. In this article, we addressed this question by using in silico tools. We reviewed the literature for miRNAs whose expression is altered upon oxidative stress damage and used them in combination with various databases and software to predict common gene targets of oxidative stress-modulated miRNAs and affected pathways. Furthermore, we identified miRNAs that simultaneously target the predicted oxidative stress-modulated miRNA gene targets. This generated a list of novel candidate miRNAs potentially involved in oxidative stress responses. By literature search and grouping of pathways and cellular responses, we could classify these candidate miRNAs and their targets into a larger scheme related to oxidative stress responses. To further exemplify the potential of our approach in free radical research, we used our explorative tools in combination with ingenuity pathway analysis to successfully identify new candidate miRNAs involved in the ubiquitination process, a master regulator of cellular responses to oxidative stress and proteostasis. Lastly, we demonstrate that our approach may also be useful to identify novel candidate connections between oxidative stress-related miRNAs and autophagy. In summary, our results indicate novel and important aspects with regard to the integrated biological roles of oxidative stress-modulated miRNAs and demonstrate how this type of in silico approach can be useful as a starting point to generate hypotheses and guide further research on the interrelation between miRNA-based gene regulation, oxidative stress signaling pathways, and autophagy.

Indexed as

AutophagyMicroRNAsOxidative StressSignal TransductionMicroRNAs

Identifiers

PMID29849898
PMCPMC5932428

What OpenQuestion holds

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LicenceCC BY
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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.