Evidence map›Paper›PMID 31805673›Full record

ReviewNutrients2019

Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review.

Gaetana Napolitano, Gianluca Fasciolo, Sergio Di Meo, Paola Venditti

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 74 citations in OpenAlex.

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  9. Targeting mitochondrial function as a potential therapeutic approach for allergic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    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

4 authors at 2 institutions in 1 country.

Gaetana NapolitanoDipartimento di Scienze e Tecnologie, Università degli Studi di Napoli Parthenope, via Acton n. 38, I-0133 Napoli, Italy.
Gianluca FascioloDipartimento di Biologia, Università di Napoli Federico II, Complesso Universitario Monte Sant'Angelo, Via Cinthia, I-80126 Napoli, Italy.
Sergio Di MeoDipartimento di Biologia, Università di Napoli Federico II, Complesso Universitario Monte Sant'Angelo, Via Cinthia, I-80126 Napoli, Italy.
Paola VendittiDipartimento di Biologia, Università di Napoli Federico II, Complesso Universitario Monte Sant'Angelo, Via Cinthia, I-80126 Napoli, Italy.
Istituto Nazionale di Fisica Nucleare, Sezione di Napoli · ITParthenope University of Naples · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are both the main sites of production and the main target of reactive oxygen species (ROS). This can lead to mitochondrial dysfunction with harmful consequences for the cells and the whole organism, resulting in metabolic and neurodegenerative disorders such as type 2 diabetes, obesity, dementia, and aging. To protect themselves from ROS, mitochondria are equipped with an efficient antioxidant system, which includes low-molecular-mass molecules and enzymes able to scavenge ROS or repair the oxidative damage. In the mitochondrial membranes, a major role is played by the lipid-soluble antioxidant vitamin E, which reacts with the peroxyl radicals faster than the molecules of polyunsaturated fatty acids, and in doing so, protects membranes from excessive oxidative damage. In the present review, we summarize the available data concerning the capacity of vitamin E supplementation to protect mitochondria from oxidative damage in hyperthyroidism, a condition that leads to increased mitochondrial ROS production and oxidative damage. Vitamin E supplementation to hyperthyroid animals limits the thyroid hormone-induced increases in mitochondrial ROS and oxidative damage. Moreover, it prevents the reduction of the high functionality components of the mitochondrial population induced by hyperthyroidism, thus preserving cell function.

Indexed as

AnimalsAntioxidantsDietary SupplementsDisease Models, AnimalHumansHyperthyroidismLiverMitochondriaMyocardiumOxidation-ReductionOxidative StressRatsReactive Oxygen SpeciesThyroid GlandVitamin EAntioxidantsReactive Oxygen SpeciesVitamin Ecold exposurehyperthyroidismmitochondriavitamin E

Identifiers

PMID31805673
PMCPMC6950234
OpenAlexW2990768483

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.