ArticleOxidative medicine and cellular longevity2022
Activation of the P62-Keap1-NRF2 Pathway Protects against Ferroptosis in Radiation-Induced Lung Injury.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review.Heart failure reviews · 2024Pooled it
- Exploring Ferroptosis: A Key Mechanism in Respiratory System Diseases and its Therapeutic Potential.Applied biochemistry and biotechnology · 2026Review
- Ionizing radiation promotes lung injury by inducing ferroptosis-driven senescence in epithelial cells via NCOA4-mediated ferritinophagy.Redox biology · 2026Article
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- Molecular mechanisms and network interactions in radiation-induced lung injury.Frontiers in physiology · 2026Review
- Ferroptosis and Radiotherapy in Lung Cancer.Cells · 2025Review
- Alpha-linolenic acid protects against heatstroke-induced acute lung injury by inhibiting ferroptosis through Nrf2 activation.Redox report : communications in free radical research · 2025Article
- Caffeic acid alleviates myocardial ischemia-reperfusion injury by directly targeting Keap1Journal of pharmaceutical analysis · 2025Article
- Novel Therapeutics for Hepatocellular Carcinoma.Clinics in liver disease · 2025Review
- LRRK2 Mediates α-Synuclein-Induced Neuroinflammation and Ferroptosis through the p62-Keap1-Nrf2 Pathway in Parkinson's Disease.Inflammation · 2025Article
- Role of Ferroptosis on Lung Epithelial Cells in Disease Progression and Treatment: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- From mitochondrial dysregulation to ferroptosis: Exploring new strategies and challenges in radioimmunotherapy (Review).International journal of oncology · 2025Review
- Unveiling pharmacological targets of Rihimaside C for radiation-induced lung injury: An in silico and experimental integrated approach.Journal of traditional and complementary medicine · 2025Article
- Baicalin plays a protective role by regulating ferroptosis in multiple diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Ferroptosis induced by environmental pollutants and its health implications.Cell death discovery · 2025Review
- Ferroptosis: a double-edged sword that enhances radiation sensitivity and facilitates radiation-induced injury in tumors.Frontiers in immunology · 2025Review
- Molecular mechanisms and potential implications of ferroptosis, cuproptosis, and disulfidptosis in septic lung injury.Frontiers in medicine · 2025Review
- Lactoferrin Modulates Radiation Response Under Hypoxic Conditions, Possibly Through the Regulation of ROS Production in a Cell Type-Specific Manner.Antioxidants (Basel, Switzerland) · 2024Article
- New insights into crosstalk between Nrf2 pathway and ferroptosis in lung disease.Cell death & disease · 2024Review
- The regulation and function of Nrf2 signaling in ferroptosis-activated cancer therapy.Acta pharmacologica Sinica · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiation-induced lung injury (RILI) is one of the most common, serious, and dose-limiting toxicities of thoracic radiotherapy. A primary cause for this is the radiation-induced cell death. Ferroptosis is a recently recognized form of regulated cell death, characterized by the accumulation of lipid peroxidation products and lethal reactive oxygen species (ROS). The ROS generated by irradiation might be the original trigger of ferroptosis in RILI. In addition, activation of the P62-Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (NRF2) pathway has been shown to blunt ferroptosis and thus acts as a protective factor. Therefore, this study aimed to explore the protective effect of the P62-Keap1-NRF2 pathway against radiation-induced ferroptosis in alveolar epithelial cells. First, we found that radiation induced ferroptosis in vitro using a RILI cell model, which could be significantly reduced by ferrostatin-1 (Fer-1), a specific ferroptosis inhibitor. Additionally, overexpression of P62 interacted with Keap1 to facilitate the translocation of NRF2 into the nucleus and promote the expression of its target proteins, including quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HO1), and ferritin heavy chain 1 (FTH1). In summary, our results demonstrated that the activation of the P62-Keap1-NRF2 pathway prevents radiation-induced ferroptosis in RILI cells, providing a theoretical basis of finding a potential therapeutic approach for RILI.
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