Ferroptosis is an iron-dependent, programmed cell death caused by the accumulation of intracellular lipid peroxidation. In recent years, increasing numbers of studies have shown that ferroptosis is key for the regulation of the homeostasis of cellular oxidative stress, cellular metabolism, and immune responses, and plays a key role in the physiological and pathological processes of multiple systems. It is currently believed that ferroptosis can inhibit tumor growth and increase the sensitivity of various tumors to chemotherapeutic drugs and immunotherapy. At the same time, ferroptosis causes normal tissue and organ damage directly involved in the occurrence and development of diseases, such as cardiovascular and cerebrovascular diseases and neurodegenerative diseases.

Oxidative stress plays a major role in activating several pathways, including ferroptosis, an iron-driven cell death characterized by iron accumulation and excessive lipid peroxidation. Strong intracellular oxidative stress, usually in the form of reactive oxygen species (ROS), is a direct factor in the occurrence of ferroptosis. Oxidative stress in cells is often pathologically exacerbated by a variety of diseases, and this property can be exploited. For example, the properties of high oxidative stress are exploited in cancer to induce ferroptosis to kill cancer. In nerve and reperfusion injury, the disease is alleviated by eliminating oxidative stress and thereby preventing the occurrence of ferroptosis.

The aim of this Special Issue is to target ferroptosis, to explore the role of ferroptosis in disease occurrence and progression and the mechanism of its regulation, and to develop inhibitors and inducers for ferroptosis, which will help us to open up new opportunities in clinical practice and disease treatment. More ideas and directions provide more choices for the protection of human health. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

• Biomarkers of ferroptosis and oxidative stress
• Mitochondria and ferroptosis
• Ferroptosis and lipid metabolism
• Targeted therapy of ferroptosis
• Ferroptosis and organ damage
• Ferroptosis and inflammation
• Ferroptosis and immunity
• Ferroptosis regulatory genes
• Lipid peroxidation and iron metabolism
• Development and application of ferroptosis inhibitors and inducers
• Ferroptosis and cellular signaling
• Ferroptosis and homeostasis of cellular oxidative stress