ReviewPharmaceutical research2010
Nrf2-Keap1 signaling as a potential target for chemoprevention of inflammation-associated carcinogenesis.
Review in Pharmaceutical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.
- The relationship between vaginal microenvironment and pelvic dysfunctional diseases in Chinese women: a systematic review and meta-analysis.International urogynecology journal · 2023Pooled it
- NAD + in fatty liver disease: mechanistic insights and associated targets.Cell biology and toxicology · 2025Review
- Proline-rich 15 depletion enhances Nrf2 cascade to promote osteoblast survival from oxidative injury.Communications biology · 2025Article
- Curcumin mimics of potential chemoprevention with NQO1 induction properties.Scientific reports · 2025Article
- The Potential of Nanotechnology in Anti-cancer Drug to Regulate Nrf2 Signaling for Cancer Therapeutic Purposes.Current medicinal chemistry · 2025Review
- Antiinflammatory effects of cucurbitacins and sorafenib in Hepg2 cells by modulating the IκB/NF-κB/COX-2 pathway through Akt signaling.Turkish journal of biology = Turk biyoloji dergisi · 2025Article
- Designing Dual-Responsive Drug Delivery Systems: The Role of Phase Change Materials and Metal-Organic Frameworks.Materials (Basel, Switzerland) · 2024Review
- Advances in Nrf2 Signaling Pathway by Targeted Nanostructured-Based Drug Delivery Systems.Biomedicines · 2024Review
- Nrf2/HO-1 signaling activation alleviates cigarette smoke-induced inflammation in chronic obstructive pulmonary disease by suppressing NLRP3-mediated pyroptosis.Journal of cardiothoracic surgery · 2024Article
- Article
- The Triterpenoid CDDO-Methyl Ester Redirects Macrophage Polarization and Reduces Lung Tumor Burden in a Nrf2-Dependent Manner.Antioxidants (Basel, Switzerland) · 2023Article
- Gallic Acid Ameliorates Aspergillus Fumigatus Keratitis Through Reducing Fungal Load and Suppressing the Inflammatory Response.Investigative ophthalmology & visual science · 2022Article
- Nrf2 signaling activation by a small molecule activator compound 16 inhibits hydrogen peroxide-induced oxidative injury and death in osteoblasts.Cell death discovery · 2022Article
- Metformin alleviates chronic obstructive pulmonary disease and cigarette smoke extract-induced glucocorticoid resistance by activating the nuclear factor E2-related factor 2/heme oxygenase-1 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Four-Octyl Itaconate Protects Chondrocytes against HOxidative medicine and cellular longevity · 2022Article
- Nuclear Factor Erythroid 2-related Factor 2 Knockout Suppresses the Development of Aggressive Colorectal Cancer Formation Induced by Azoxymethane/Dextran Sulfate Sodium-Treatment in Female Mice.Journal of cancer prevention · 2021Article
- Drug delivery nanocarriers and recent advances ventured to improve therapeutic efficacy against osteosarcoma: an overview.Journal of the Egyptian National Cancer Institute · 2021Review
- Solid Lipid Particles for Lung Metastasis Treatment.Pharmaceutics · 2021Article
- An Overview of Nrf2 Signaling Pathway and Its Role in Inflammation.Molecules (Basel, Switzerland) · 2020Review
- A Novel Kelch-Like-1 Is Involved in Antioxidant Response by Regulating Antioxidant Enzyme System inGenes · 2020Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent inflammatory tissue damage is causally associated with each stage of carcinogenesis. Inflammation-induced generation of reactive oxygen species, reactive nitrogen species, and other reactive species not only cause DNA damage and subsequently mutations, but also stimulate proliferation of initiated cells and even metastasis and angiogenesis. Induction of cellular cytoprotective enzymes (e.g., heme oxygenase-1, NAD(P)H:quinone oxidoreductase, superoxide dismutase, glutathione-S-transferase, etc.) has been shown to mitigate aforementioned events implicated in inflammation-induced carcinogenesis. A unique feature of genes encoding these cytoprotective enzymes is the presence of a cis-acting element, known as antioxidant response element (ARE) or electrophile response element (EpRE), in their promoter region. A stress-responsive transcription factor, nuclear factor erythroid-2-related factor-2 (Nrf2), initially recognized as a key transcriptional regulator of various cytoprotective enzymes, is known to play a pivotal role in cellular defense against inflammatory injuries. Activation of Nrf2 involves its release from the cytosolic repressor Kelch-like ECH-associated protein-1 (Keap1) and subsequent stabilization and nuclear localization for ARE/EpRE binding. Genetic or pharmacologic inactivation of Nrf2 has been shown to abolish cytoprotective capability and to aggravate experimentally induced inflammatory injuries. Thus, Nrf2-mediated cytoprotective gene induction is an effective strategy for the chemoprevention of inflammation-associated carcinogenesis.
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Registered trials
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.