Evidence map›Paper›PMID 29187515›Full record

ReviewPhysiological genomics2018

Nrf2 at the heart of oxidative stress and cardiac protection.

Qin M Chen, Anthony J Maltagliati

Open access · bronzeAbstract readReview
In one paragraph

Review in Physiological genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
248citing papers in PubMed, 3 pooled it
9.1field-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

248 citing papers in PubMed, 3 syntheses or guidelines pooled it, 475 citations in OpenAlex.

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  20. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review

188 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

2 authors at 1 institution in 1 country.

Qin M ChenDepartment of Pharmacology, College of Medicine, University of Arizona , Tucson, Arizona.
Anthony J MaltagliatiDepartment of Pharmacology, College of Medicine, University of Arizona , Tucson, Arizona.
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Teri L Bankhead · 1985 to 2026
$110.2M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Translation Control of Oxidative StressR01GM111337 · NIGMS · UNIVERSITY OF ARIZONA · PI CHEN, QIN M · 2014 to 2016
$803k
NCI NIH HHS P30 CA023074NIEHS NIH HHS P30 ES006694NIGMS NIH HHS R01 GM111337
6 · The paper itself

Abstract

The NFE2L2 gene encodes the transcription factor Nrf2 best known for regulating the expression of antioxidant and detoxification genes. Gene knockout approaches have demonstrated its universal cytoprotective features. While Nrf2 has been the topic of intensive research in cancer biology since its discovery in 1994, understanding the role of Nrf2 in cardiovascular disease has just begun. The literature concerning Nrf2 in experimental models of atherosclerosis, ischemia, reperfusion, cardiac hypertrophy, heart failure, and diabetes supports its cardiac protective character. In addition to antioxidant and detoxification genes, Nrf2 has been found to regulate genes participating in cell signaling, transcription, anabolic metabolism, autophagy, cell proliferation, extracellular matrix remodeling, and organ development, suggesting that Nrf2 governs damage resistance as well as wound repair and tissue remodeling. A long list of small molecules, most derived from natural products, have been characterized as Nrf2 inducers. These compounds disrupt Keap1-mediated Nrf2 ubquitination, thereby prohibiting proteasomal degradation and allowing Nrf2 protein to accumulate and translocate to the nucleus, where Nrf2 interacts with sMaf to bind to ARE in the promoter of genes. Recently alternative mechanisms driving Nrf2 protein increase have been revealed, including removal of Keap1 by autophagy due to p62/SQSTM1 binding, inhibition of βTrCP or Synoviolin/Hrd1-mediated ubiquitination of Nrf2, and de novo Nrf2 protein translation. We review here a large volume of literature reporting historical and recent discoveries about the function and regulation of Nrf2 gene. Multiple lines of evidence presented here support the potential of dialing up the Nrf2 pathway for cardiac protection in the clinic.

Indexed as

AnimalsBiological ProductsGene Expression RegulationHumansMyocardiumNF-E2-Related Factor 2Oxidative StressSignal TransductionBiological ProductsNF-E2-Related Factor 2antioxidant response elementischemia and reperfusionnatural productsprotein translationubiquitination

Identifiers

PMID29187515
PMCPMC5867612
OpenAlexW2769077130

What OpenQuestion holds

Textmetadata
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.