Ferroptosis and Cellular Aging: A Comprehensive Analysis of Iron-Induced Lipid Peroxidation in Cellular Senescence and Its Impact on Age-Related Disease Development

Background: Ferroptosis is a distinct, tightly regulated form of cell death that depends on iron and lipid peroxidation. Emerging research points to its critical involvement in aging and the development of age-associated conditions such as neurodegenerative disorders, cardiovascular diseases, and certain cancers. Objective: This review aims to examine the molecular basis of ferroptosis and its impact on agingrelated cellular deterioration. Gaining insights into these pathways may facilitate the identification of novel therapeutic targets for slowing aging and managing related diseases. Methods: An in-depth review of recent scientific literature was conducted, focusing on the core mechanisms of ferroptosis—namely, iron overload, oxidative stress, lipid peroxidation, and the depletion of glutathione. Emphasis was placed on studies linking these processes to cellular dysfunction in neurons, heart muscle cells, and epithelial tissues during aging. Results: Findings suggest that ferroptosis becomes more prominent as antioxidant defenses weaken and iron dysregulation intensifies with age. This promotes neuronal injury in neurodegenerative conditions and impairs vascular cell integrity in cardiovascular diseases. The deterioration of regulatory systems involved in ferroptosis contributes to tissue damage and a decline in organ function. Discussion: The interplay between ferroptosis and aging underscores the need for further research into targeted interventions that could modulate this pathway. Conclusion: Ferroptosis is a significant contributor to the cellular and molecular changes seen in aging and age-related diseases. Understanding its complex regulation offers promising avenues for therapeutic development aimed at mitigating the effects of aging and preventing associated health conditions.