Ferroptosis: Molecular Mechanisms of Regulation and Therapeutic Potential in the Pathogenesis of Multifactorial Diseases

Ferroptosis is a novel form of regulated cell death that plays a key role in the pathogenesis of a wide range of multifactorial diseases. Its uniqueness lies in the iron-dependent accumulation of lipid peroxides, which distinguishes it from apoptosis, necroptosis, and autophagy. Understanding the molecular mechanisms of ferroptosis opens up new therapeutic prospects, but the dual role of this process – both as a factor of malignant cell death and a mediator of tissue damage – creates significant challenges for clinical application. The paper systematizes current ideas about the molecular mechanisms of ferroptosis regulation, including iron metabolism, lipid peroxidation, and antioxidant defense systems. Signaling pathways that modulate sensitivity to ferroptosis are analyzed. Particular attention is paid to the dual role of ferroptosis in the pathogenesis of diseases: induction of ferroptosis is considered a promising strategy for overcoming the resistance of malignant neoplasms to chemotherapy, immunotherapy and radiotherapy, while its inhibition is critical for protecting tissues from ischemia-reperfusion injury, neurodegeneration and inflammation. Key counterarguments are highlighted, in particular the pro-inflammatory and immunosuppressive effects of ferroptosis, which may contribute to tumor progression. Ferroptosis is a universal mechanism of cell death with powerful therapeutic potential, however, its clinical implementation requires a differentiated approach depending on the pathological context. Promising directions are the development of highly selective modulators, identification of specific biomarkers of ferroptosis in vivo and conducting well-designed clinical trials. In-depth study of molecular regulatory networks will allow translating fundamental knowledge into personalized treatment strategies for multifactorial diseases.