Evidence map›Paper›PMID 24810054›Full record

ArticleCell death & disease2014

Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death.

X Zou, J Gao, Y Zheng, X Wang, C Chen, K Cao, J Xu, Y Li, W Lu, J Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 100 citations in OpenAlex.

  1. Lute-GenAntioxidants (Basel, Switzerland) · 2026
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  8. BlingLifeJournal of microbiology and biotechnology · 2025
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  19. Induction of the antioxidant defense system using long-chain carotenoids extracted from extreme halophilic archaeon, Halovenus aranensis.International microbiology : the official journal of the Spanish Society for Microbiology · 2022
    Article
  20. Review
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

11 authors at 2 institutions in 1 country.

X Zou1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Translational Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
J Gao1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
Y ZhengJinan Central Hospital Affiliated to Shandong University, Jinan, China.
X Wang1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
C Chen1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
K Cao1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
J Xu1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
Y Li1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
W Lu1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Translational Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
J Liu1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
Z Feng1] Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China [2] Center for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, FIST, Xi'an Jiaotong University, Xi'an, China.
Xi'an Jiaotong University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zeaxanthin (Zea) is a major carotenoid pigment contained in human retina, and its daily supplementation associated with lower risk of age-related macular degeneration. Despite known property of Zea as an antioxidant, its underlying molecular mechanisms of action remain poorly understood. In this study, we aim to study the regulation mechanism of Zea on phase II detoxification enzymes. In normal human retinal pigment epithelium cells, Zea promoted the nuclear translocation of NF-E2-related factor 2 (Nrf2) and induced mRNA and protein expression of phase II enzymes, the induction was suppressed by specific knockdown of Nrf2. Zea also effectively protected against tert-butyl hydroperoxide-induced mitochondrial dysfunction and apoptosis. Glutathione (GSH) as the most important antioxidant was also induced by Zea through Nrf2 activation in a time- and dose-dependent manner, whereas the protective effects of Zea were decimated by inhibition of GSH synthesis. Finally, Zea activated the PI3K/Akt and MAPK/ERK pathway, whereas only PI3K/Akt activation correlated with phase II enzymes induction and Zea protection. In further in vivo analyses, Zea showed effects of inducing phase II enzymes and increased GSH content, which contributed to the reduced lipid and protein peroxidation in the retina as well as the liver, heart, and serum of the Sprague-Dawley rats. For the first time, Zea is presented as a phase II enzymes inducer instead of being an antioxidant. By activating Nrf2-mediated phase II enzymes, Zea could enhance anti-oxidative capacity and prevent cell death both in vivo and in vitro.

Indexed as

Active Transport, Cell NucleusAnimalsAntioxidantsApoptosisCell LineCytoprotectionDose-Response Relationship, DrugEnzyme InductionExtracellular Signal-Regulated MAP KinasesGlutathioneGlutathione PeroxidaseGlutathione TransferaseHumansLipid PeroxidationLiverMaleAntioxidantsExtracellular Signal-Regulated MAP KinasesGlutathioneGlutathione PeroxidaseGlutathione TransferaseNFE2L2 protein, humanNF-E2-Related Factor 2OxidantsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRNA, MessengerSuperoxide DismutaseXanthophyllsZeaxanthins

Identifiers

PMID24810054
PMCPMC4047913
OpenAlexW2090792221

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.