Ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, is intricately linked to ageing and cellular senescence. Understanding and modulating ferroptosis may offer novel ways to address age-related diseases, improve healthspan, and promote longevity by reducing tissue dysfunction and enhancing overall well-being.
November 2024 – Heliyon
Key takeaways
- Ferroptosis drives ageing-related tissue damage: Iron-dependent lipid peroxidation triggers cell death, contributing to age-related decline and tissue dysfunction. Over time, this process accelerates chronic diseases, making ferroptosis a key player in ageing. Reducing oxidative stress and balancing iron levels could help mitigate its effects and promote healthier ageing
- Cellular senescence and ferroptosis are linked: Senescent cells accumulate excess iron, making them resistant to ferroptosis while promoting inflammation and tissue damage. However, targeting ferroptosis in specific ways may help clear senescent cells, offering a potential strategy to delay ageing and improve cellular function
- Iron balance is crucial for longevity: Both iron deficiency and excess drive ageing-related issues. While too little iron impairs energy production, excess iron fuels oxidative damage and ferroptosis. Regulating iron metabolism through diet, supplementation, or chelation therapies may optimise healthspan and reduce age-related disease risk
- Ferroptosis modulation may slow ageing: Controlling lipid peroxidation and enhancing antioxidant defences could protect cells from ferroptotic death. Nutrients like selenium, glutathione, and coenzyme Q10, as well as targeted therapies, might reduce ferroptosis-related damage and promote longevity
Read the article at: De Leon-Oliva, Diego, et al. “Improving Understanding of Ferroptosis: Molecular Mechanisms, Connection with Cellular Senescence and Implications for Aging.” Heliyon, vol. 10, 2024, e39684, https://doi.org/10.1016/j.heliyon.2024.e39684.
