Evidence map›Paper›PMID 34332753›Full record

ReviewTrends in pharmacological sciences2021

Nrf2 for cardiac protection: pharmacological options against oxidative stress.

Qin M Chen

Open access · greenAbstract readReview
In one paragraph

Review in Trends in pharmacological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
9.3field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.

  1. Pooled it
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  15. Vericiguat reduces pyroptosis in rats with coronary microembolization by inhibiting the AMPK/Nrf2/NLRP3 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
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11 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

1 author at 1 institution in 1 country.

Qin M ChenDepartment of Pharmacy Practice and Science, College of Pharmacy, University of Arizona, Tucson, AZ 85721, USA. Electronic address: qchen@email.arizona.edu.
University of Arizona · US

Funding

Nrf2 Protein Translation for Protection Against Tissue InjuryR01GM126165 · NIGMS · UNIVERSITY OF ARIZONA · PI CHEN, QIN M · 2018 to 2021
$1.7M
Mechanism and Function of Stress Induced Protein TranslationR01GM125212 · NIGMS · UNIVERSITY OF ARIZONA · PI CHEN, QIN M · 2018 to 2021
$1.4M
Translational Control of Oxidative Stress in Myocardial InfarctionR01HL089958 · NHLBI · UNIVERSITY OF ARIZONA · PI CHEN, QIN M · 2009 to 2010
$908k
Translation Control of Oxidative StressR01GM111337 · NIGMS · UNIVERSITY OF ARIZONA · PI CHEN, QIN M · 2014 to 2016
$803k
NHLBI NIH HHS R01 HL089958NIGMS NIH HHS R01 GM111337NIGMS NIH HHS R01 GM125212NIGMS NIH HHS R01 GM126165
6 · The paper itself

Abstract

Myocardial ischemia or reperfusion increases the generation of reactive oxygen species (ROS) from damaged mitochondria, NADPH oxidases, xanthine oxidase, and inflammation. ROS can be removed by eight endogenous antioxidant and redox systems, many components of which are expressed under the influence of the activated Nrf2 transcription factor. Transcriptomic profiling, sequencing of Nrf2-bound DNA, and Nrf2 gene knockout studies have revealed the power of Nrf2 beyond the antioxidant and detoxification response, from tissue recovery, repair, and remodeling, mitochondrial turnover, and metabolic reprogramming to the suppression of proinflammatory cytokines. Multifaceted regulatory mechanisms for Nrf2 protein levels or activity have been mapped to its functional domains, Nrf2-ECH homology (Neh)1-7. Oxidative stress activates Nrf2 via nuclear translocation, de novo protein translation, and increased protein stability due to removal of the Kelch-like ECH-associated protein 1 (Keap1) checkpoint, or the inactivation of β-transducin repeat-containing protein (β-TrCP), or Hmg-CoA reductase degradation protein 1 (Hrd1). The promise of small-molecule Nrf2 inducers from natural products or derivatives is discussed here. Experimental evidence is presented to support Nrf2 as a lead target for drug development to further improve the treatment outcome for myocardial infarction (MI).

Indexed as

NF-E2-Related Factor 2Oxidative StressAntioxidantsHumansKelch-Like ECH-Associated Protein 1Reactive Oxygen SpeciesAntioxidantsKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Reactive Oxygen Speciesinflammationmitochondriamyocardial ischemiareperfusionsmall moleculetranscription factor

Identifiers

PMID34332753
PMCPMC8785681
OpenAlexW3184404755

What OpenQuestion holds

Textmetadata
LicenceTDM
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.