Evidence map›Paper›PMID 29074861›Full record

ArticleScientific reports2017

Sulforaphane reactivates cellular antioxidant defense by inducing Nrf2/ARE/Prdx6 activity during aging and oxidative stress.

Eri Kubo, Bhavana Chhunchha, Prerna Singh, Hiroshi Sasaki, Dhirendra P Singh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

119 citing papers in PubMed, 220 citations in OpenAlex.

  1. Trial
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  4. Genetic and pharmacologic modulations elucidate NRF2 protective role in acute pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
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  8. Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026
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59 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 2 institutions in 2 countries.

Eri KuboDepartment of Ophthalmology, Kanazawa Medical University, Kanazawa, Japan. kuboe@kanazawa-med.ac.jp.
Bhavana ChhunchhaDepartment of Ophthalmology and Visual Science, University of Nebraska Medical Center, NE, Omaha, USA.
Prerna SinghDepartment of Ophthalmology and Visual Science, University of Nebraska Medical Center, NE, Omaha, USA.
Hiroshi SasakiDepartment of Ophthalmology, Kanazawa Medical University, Kanazawa, Japan.
Dhirendra P SinghDepartment of Ophthalmology and Visual Science, University of Nebraska Medical Center, NE, Omaha, USA. dpsingh@unmc.edu.
University of Nebraska Medical Center · USKanazawa Medical University · JP

Funding

Regulation and Function of Prdx6 in eye lens during Aging & Oxidative StressR01EY024589 · NEI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SINGH, DHIRENDRA P · 2014 to 2018
$1.9M
NEI NIH HHS R01 EY024589
6 · The paper itself

Abstract

Upon oxidative stress and aging, Nrf2 (NFE2-related factor2) triggers antioxidant defense genes to defends against homeostatic failure. Using human(h) or rat(r) lens epithelial cells (LECs) and aging human lenses, we showed that a progressive increase in oxidative load during aging was linked to a decline in Prdx6 expression. DNA binding experiments using gel-shift and ChIP assays demonstrated a progressive reduction in Nrf2/ARE binding (-357/-349) of Prdx6 promoter. The promoter (-918) with ARE showed a marked reduction in young vs aged hLECs, which was directly correlated to decreased Nrf2/ARE binding. A Nrf2 activator, Sulforaphane (SFN), augmented Prdx6, catalase and GSTπ expression in dose-dependent fashion, and halted Nrf2 dysregulation of these antioxidants. SFN reinforced Nrf2/DNA binding and increased promoter activities by enhancing expression and facilitating Nrf2 translocalization in nucleus. Conversely, promoter mutated at ARE site did not respond to SFN, validating the SFN-mediated restoration of Nrf2/ARE signaling. Furthermore, SFN rescued cells from UVB-induced toxicity in dose-dependent fashion, which was consistent with SFN's dose-dependent activation of Nrf2/ARE interaction. Importantly, knockdown of Prdx6 revealed that Prdx6 expression was prerequisite for SFN-mediated cytoprotection. Collectively, our results suggest that loss of Prdx6 caused by dysregulation of ARE/Nrf2 can be attenuated through a SFN, to combat diseases associated with aging.

Indexed as

Active Transport, Cell NucleusAdolescentAdultAgedAgingAnimalsAntioxidantsCell NucleusDose-Response Relationship, DrugGene Expression RegulationHumansIsothiocyanatesMiddle AgedNF-E2-Related Factor 2Oxidative StressPeroxiredoxin VIAntioxidantsIsothiocyanatesNF-E2-Related Factor 2Peroxiredoxin VIPrdx6 protein, ratsulforaphaneSulfoxides

Identifiers

PMID29074861
PMCPMC5658327
OpenAlexW2766209227

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.