ReviewInternational journal of molecular sciences2023
Mitigation of Cardiovascular Disease and Toxicity through NRF2 Signalling.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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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.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Hass Avocado Bioactive Compounds Attenuating Oxidative Stress and Inflammation in Ischemia-reperfusion Injury: An Integrative Review.Plant foods for human nutrition (Dordrecht, Netherlands) · 2026Review
- Sex-based differences in the NRF2 oxidative stress response: Implications for precision therapeutics.Redox biology · 2026Review
- Transcriptomic biomarkers related to cardiac disease in childhood cancer survivors: a case-control study.European heart journal · 2026Article
- Nuclear factor erythroid 2 related factor 2, tumor necrosis factor alpha, interleukin-40, and endorepellin levels in patients undergoing coronary artery bypass grafting.Revista da Associacao Medica Brasileira (1992) · 2026Article
- Sex-Specific Association between HO-1 (GT)n Promoter Polymorphism and Large-Artery Atherosclerosis Stroke.Journal of atherosclerosis and thrombosis · 2025Article
- Environmental Toxins and Oxidative Stress: The Link to Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Small Molecules Targeting Mitochondria: A Mechanistic Approach to Combating Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2025Review
- Recent advancements and comprehensive analyses of butyric acid in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Redox Imbalance and Antioxidant Defenses Dysfunction: Key Contributors to Early Aging in Childhood Cancer Survivors.Antioxidants (Basel, Switzerland) · 2024Article
- Targeting Nrf2/PHKG2 axis to enhance radiosensitivity in NSCLC.NPJ precision oncology · 2024Article
- Personalized Approaches to Cardiovascular Disease: Insights into FDA-Approved Interventions and Clinical Pharmacogenetics.Current pharmaceutical design · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiovascular toxicity and diseases are phenomena that have a vastly detrimental impact on morbidity and mortality. The pathophysiology driving the development of these conditions is multifactorial but commonly includes the perturbance of reactive oxygen species (ROS) signalling, iron homeostasis and mitochondrial bioenergetics. The transcription factor nuclear factor erythroid 2 (NFE2)-related factor 2 (NRF2), a master regulator of cytoprotective responses, drives the expression of genes that provide resistance to oxidative, electrophilic and xenobiotic stresses. Recent research has suggested that stimulation of the NRF2 signalling pathway can alleviate cardiotoxicity and hallmarks of cardiovascular disease progression. However, dysregulation of NRF2 dynamic responses can be severely impacted by ageing processes and off-target toxicity from clinical medicines including anthracycline chemotherapeutics, rendering cells of the cardiovascular system susceptible to toxicity and subsequent tissue dysfunction. This review addresses the current understanding of NRF2 mechanisms under homeostatic and cardiovascular pathophysiological conditions within the context of wider implications for this diverse transcription factor.
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What OpenQuestion holds
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.