Evidence map›Paper›PMID 28083748›Full record

ReviewInflammopharmacology2017

Antioxidant and anti-inflammatory effects of zinc. Zinc-dependent NF-κB signaling.

Magdalena Jarosz, Magdalena Olbert, Gabriela Wyszogrodzka, Katarzyna Młyniec, Tadeusz Librowski

Open access · hybridAbstract readReview
In one paragraph

Review in Inflammopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 357 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
357citing papers in PubMed, 2 pooled it
21.9field-weighted citation impact, top 1% 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

357 citing papers in PubMed, 2 syntheses or guidelines pooled it, 688 citations in OpenAlex.

  1. Pooled it
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  10. Therapeutic potential of zinc supplementation in rheumatoid arthritis: clinical evidence, molecular mechanisms, and formulation-specific effects.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  11. Article
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  13. Associations between multiple essential trace metal concentrations and risk of hyperuricemia: insights from a central Chinese population.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  19. Observational
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297 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Magdalena JaroszDepartment of Radioligands, Jagiellonian University Medical College, Medyczna 9, 30-688, Krakow, Poland. m.gawel.87@gmail.com.ORCID http://orcid.org/0000-0002-8120-6785
Magdalena OlbertDepartment of Radioligands, Jagiellonian University Medical College, Medyczna 9, 30-688, Krakow, Poland.
Gabriela WyszogrodzkaDepartment of Pharmaceutical Technology and Biopharmaceutics, Jagiellonian University Medical College, Medyczna 9, 30-688, Krakow, Poland.
Katarzyna MłyniecDepartment of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, 30-688, Krakow, Poland.
Tadeusz LibrowskiDepartment of Radioligands, Jagiellonian University Medical College, Medyczna 9, 30-688, Krakow, Poland.
Jagiellonian University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc is a nutritionally fundamental trace element, essential to the structure and function of numerous macromolecules, including enzymes regulating cellular processes and cellular signaling pathways. The mineral modulates immune response and exhibits antioxidant and anti-inflammatory activity. Zinc retards oxidative processes on a long-term basis by inducing the expression of metallothioneins. These metal-binding cysteine-rich proteins are responsible for maintaining zinc-related cell homeostasis and act as potent electrophilic scavengers and cytoprotective agents. Furthermore, zinc increases the activation of antioxidant proteins and enzymes, such as glutathione and catalase. On the other hand, zinc exerts its antioxidant effect via two acute mechanisms, one of which is the stabilization of protein sulfhydryls against oxidation. The second mechanism consists in antagonizing transition metal-catalyzed reactions. Zinc can exchange redox active metals, such as copper and iron, in certain binding sites and attenuate cellular site-specific oxidative injury. Studies have demonstrated that physiological reconstitution of zinc restrains immune activation, whereas zinc deficiency, in the setting of severe infection, provokes a systemic increase in NF-κB activation. In vitro studies have shown that zinc decreases NF-κB activation and its target genes, such as TNF-α and IL-1β, and increases the gene expression of A20 and PPAR-α, the two zinc finger proteins with anti-inflammatory properties. Alternative NF-κB inhibitory mechanism is initiated by the inhibition of cyclic nucleotide phosphodiesterase, whereas another presumed mechanism consists in inhibition of IκB kinase in response to infection by zinc ions that have been imported into cells by ZIP8.

Indexed as

AnimalsAnti-Inflammatory AgentsAntioxidantsHumansInflammationNF-kappa BOxidative StressSignal TransductionZincAnti-Inflammatory AgentsAntioxidantsNF-kappa BZincInflammationNF-κB signalingOxidative stressProtein A20ZincZIP8

Identifiers

PMID28083748
PMCPMC5306179
OpenAlexW2579322339

What OpenQuestion holds

Textmetadata
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.