Role of ferroptosis in radiation-induced soft tissue injury.
Charlotte E BerryCarter B KendigNicholas AnAlexander Z FazilatAndrew A ChurukianMichelle GriffinPhoebe M PanMichael T LongakerScott J DixonDerrick C WanPublished in: Cell death discovery (2024)
Ionizing radiation has been pivotal in cancer therapy since its discovery. Despite its therapeutic benefits, IR causes significant acute and chronic complications due to DNA damage and the generation of reactive oxygen species, which harm nucleic acids, lipids, and proteins. While cancer cells are more vulnerable to ionizing radiation due to their inefficiency in repairing damage, healthy cells in the irradiated area also suffer. Various types of cell death occur, including apoptosis, necrosis, pyroptosis, autophagy-dependent cell death, immunogenic cell death, and ferroptosis. Ferroptosis, driven by iron-dependent lipid peroxide accumulation, has been recognized as crucial in radiation therapy's therapeutic effects and complications, with extensive research across various tissues. This review aims to summarize the pathways involved in radiation-related ferroptosis, findings in different organs, and drugs targeting ferroptosis to mitigate its harmful effects.
Keyphrases
- cell death
- cell cycle arrest
- radiation induced
- radiation therapy
- cancer therapy
- dna damage
- oxidative stress
- reactive oxygen species
- soft tissue
- induced apoptosis
- drug induced
- risk factors
- drug delivery
- small molecule
- gene expression
- endoplasmic reticulum stress
- fatty acid
- squamous cell carcinoma
- respiratory failure
- aortic dissection
- iron deficiency