Evidence map›Paper›PMID 31827671›Full record

ArticleOxidative medicine and cellular longevity2019

Increased Circulating Levels of Interleukin-6 Affect the Redox Balance in Skeletal Muscle.

Laura Forcina, Carmen Miano, Bianca M Scicchitano, Emanuele Rizzuto, Maria Grazia Berardinelli, Fabrizio De Benedetti, Laura Pelosi, Antonio Musarò

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 55 citations in OpenAlex.

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  14. Advance in the mechanism and clinical research of myalgia in long COVID.American journal of clinical and experimental immunology · 2024
    Review
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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

8 authors at 4 institutions in 1 country.

Laura ForcinaDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Via A. Scarpa 14, 00161 Rome, Italy.ORCID https://orcid.org/0000-0003-3446-7672
Carmen MianoDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Via A. Scarpa 14, 00161 Rome, Italy.
Bianca M ScicchitanoIstituto di Istologia ed Embriologia, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario "Agostino Gemelli", IRCCS, 00168 Roma, Italy.ORCID https://orcid.org/0000-0002-9599-6642
Emanuele RizzutoDepartment of Mechanical and Aerospace Engineering, Sapienza University of Rome, 00184 Rome, Italy.ORCID https://orcid.org/0000-0003-2314-6128
Maria Grazia BerardinelliDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Via A. Scarpa 14, 00161 Rome, Italy.
Fabrizio De BenedettiDivision of Rheumatology and Immuno-Rheumatology Research Laboratories, Bambino Gesù Children's Hospital, 00146 Rome, Italy.
Laura PelosiDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Via A. Scarpa 14, 00161 Rome, Italy.ORCID https://orcid.org/0000-0003-3964-8157
Antonio MusaròDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Via A. Scarpa 14, 00161 Rome, Italy.ORCID https://orcid.org/0000-0002-2944-9739
Istituto Pasteur · ITBambino Gesù Children's Hospital · ITSapienza University of Rome · ITUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extent of oxidative stress and chronic inflammation are closely related events which coexist in a muscle environment under pathologic conditions. It has been generally accepted that the inflammatory cells, as well as myofibers, are sources of reactive species which are, in turn, able to amplify the activation of proinflammatory pathways. However, the precise mechanism underlining the physiopathologic interplay between ROS generation and inflammatory response has to be fully clarified. Thus, the identification of key molecular players in the interconnected pathogenic network between the two processes might help to design more specific therapeutic approaches for degenerative diseases. Here, we investigated whether elevated circulating levels of the proinflammatory cytokine Interleukin-6 (IL-6) are sufficient to perturb the physiologic redox balance in skeletal muscle, independently of tissue damage and inflammatory response. We observed that the overexpression of circulating IL-6 enhances the generation and accumulation of free radicals in the diaphragm muscle of adult NSE/IL-6 mice, by deregulating redox-associated molecular circuits and impinging the nuclear factor erythroid 2-related factor 2- (Nrf2-) mediated antioxidant response. Our findings are coherent with a model in which uncontrolled levels of IL-6 in the bloodstream can influence the local redox homeostasis, inducing the establishment of prooxidative conditions in skeletal muscle tissue.

Indexed as

AnimalsAntioxidantsHumansInterleukin-6MiceMice, Inbred C57BLMice, TransgenicMuscle, SkeletalNADPH Oxidase 2NF-E2-Related Factor 2Reactive Oxygen SpeciesSirtuin 1Superoxide Dismutase-1AntioxidantsInterleukin-6NADPH Oxidase 2NF-E2-Related Factor 2Reactive Oxygen SpeciesSirtuin 1Superoxide Dismutase-1

Identifiers

PMID31827671
PMCPMC6881749
OpenAlexW2986085155

What OpenQuestion holds

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LicenceCC BY
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.