“Ferroptosis across Major Human Diseases: Moleucular Mechanism and Therapeutic Opportunities”

Ferroptosis has emerged as a distinct form of regulated cell death characterized by iron accumulation, excessive lipid peroxidation, and disruption of cellular redox homeostasis. Unlike classical forms of cell death, including apoptosis, necroptosis, pyroptosis, and autophagy-associated cell death, ferroptosis is primarily driven by iron metabolism imbalance, oxidative stress, and failure of antioxidant defense systems. It influence the diverse physiological and pathological processes. This review provides an updated overview of the molecular mechanisms underlying ferroptosis, focusing on iron regulation, reactive oxygen species generation, lipid peroxidation pathways, glutathione depletion, glutathione peroxidase 4 (GPX4) activity, and System Xc⁻-mediated antioxidant defense. Furthermore, we explore the disease-specific roles of ferroptosis across major human disorders, including cancer, cardiovascular diseases, neurological disorders, metabolic diseases. Emerging therapeutic strategies involves ferroptosis induction or inhibition, antioxidant modulation, and nanomedicine-based delivery systems provide promising opportunities for regulation of ferroptotic pathways. However, clinical translation remains challenging due to disease-specific regulatory mechanisms, potential off-target effects, safety concerns, and limited availability of reliable biomarkers. By integrating recent mechanistic discoveries and therapeutic advances, this review highlights the significance of ferroptosis in disease biology and its potential contribution to future precision medicine strategies.