Evidence map›Paper›PMID 33652780›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Nrf2 Signaling Pathway in Chemoprotection and Doxorubicin Resistance: Potential Application in Drug Discovery.

Sepideh Mirzaei, Ali Zarrabi, Farid Hashemi, Amirhossein Zabolian, Hossein Saleki, Negar Azami, Soodeh Hamzehlou, Mahdi Vasheghani Farahani, Kiavash Hushmandi, Milad Ashrafizadeh and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.1field-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

63 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
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  9. SoloxoloneInternational journal of molecular sciences · 2025
    Article
  10. NRF2 as a ferroptosis gatekeeper in colorectal cancer: implications for therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
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3 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

12 authors at 6 institutions in 4 countries.

Sepideh MirzaeiDepartment of Biology, Faculty of Science, Islamic Azad University, Science and Research Branch, Tehran 1477893855, Iran.
Ali ZarrabiSabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla, 34956 Istanbul, Turkey.ORCID 0000-0003-0391-1769
Farid HashemiDepartment of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran 1417466191, Iran.
Amirhossein ZabolianYoung Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran 1477893855, Iran.
Hossein SalekiYoung Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran 1477893855, Iran.
Negar AzamiYoung Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran 1477893855, Iran.
Soodeh HamzehlouYoung Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran 1477893855, Iran.
Mahdi Vasheghani FarahaniYoung Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran 1477893855, Iran.
Kiavash HushmandiDivision of Epidemiology, Department of Food Hygiene and Quality Control, Faculty of Veterinary Medicine, University of Tehran, Tehran 1417466191, Iran.
Milad AshrafizadehSabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla, 34956 Istanbul, Turkey.
Haroon KhanDepartment of Pharmacy, Abdul Wali Khan University, Mardan 23200, Pakistan.
Alan Prem KumarCancer Science Institute of Singapore, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore.ORCID 0000-0002-3754-5712
Islamic Azad University Medical Branch of Tehran · IRSabancı Üniversitesi · TRUniversity of Tehran · IRAbdul Wali Khan University Mardan · PKIslamic Azad University, Science and Research Branch · IRNational University of Singapore · SG

Funding

Ministry of Education - Singapore T2EP30120-0042
6 · The paper itself

Abstract

Doxorubicin (DOX) is extensively applied in cancer therapy due to its efficacy in suppressing cancer progression and inducing apoptosis. After its discovery, this chemotherapeutic agent has been frequently used for cancer therapy, leading to chemoresistance. Due to dose-dependent toxicity, high concentrations of DOX cannot be administered to cancer patients. Therefore, experiments have been directed towards revealing underlying mechanisms responsible for DOX resistance and ameliorating its adverse effects. Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling is activated to increase levels of reactive oxygen species (ROS) in cells to protect them against oxidative stress. It has been reported that Nrf2 activation is associated with drug resistance. In cells exposed to DOX, stimulation of Nrf2 signaling protects cells against cell death. Various upstream mediators regulate Nrf2 in DOX resistance. Strategies, both pharmacological and genetic interventions, have been applied for reversing DOX resistance. However, Nrf2 induction is of importance for alleviating side effects of DOX. Pharmacological agents with naturally occurring compounds as the most common have been used for inducing Nrf2 signaling in DOX amelioration. Furthermore, signaling networks in which Nrf2 is a key player for protection against DOX adverse effects have been revealed and are discussed in the current review.

Indexed as

chemoresistancedoxorubicinnuclear factor erythroid 2-related factor 2 (Nrf2), cancer therapyoxidative stressredox signaling

Identifiers

PMID33652780
PMCPMC7996755
OpenAlexW3134069384

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.