Ferroptosis is a novel, regulated form of cell death characterized by the disruption of iron metabolism and accumulation of lipid peroxides. Inflammation is the physiological response of the host to tissue damage, and its main purpose is to restore tissue homeostasis. Recently, numerous studies have shown that ferroptosis plays an important role in the development of various inflammation-related diseases. Ferroptosis is involved in the progression of inflammation, such as acute lung injury, acute kidney injury, rheumatoid arthritis, sepsis, and neurodegenerative diseases.

Iron-dependent oxidative stress and lipid peroxidation are common features of ferroptosis and inflammatory diseases, and there is compelling evidence that several antioxidants that function as ferroptosis inhibitors have anti-inflammatory effects in experimental models of certain diseases. The nuclear factor erythroid 2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signaling axis is a multi-organ protective chain that protects against oxidative stress damage. This signaling axis regulates anti-inflammatory and antioxidant activity by regulating mitochondrial oxidative stress and ferroptosis.

The aim of this Special Issue is to explore the role and regulation mechanism of ferroptosis in inflammation-related diseases, and screen new biomarkers and developing inhibitors for ferroptosis to help us find more directions in the treatment of inflammation-related diseases. Original research and review articles are welcomed.

Potential topics include but are not limited to the following:

• Ferroptosis and inflammatory bowel disease
• Ferroptosis and acute lung injury
• Ferroptosis and acute kidney injury
• Ferroptosis in sepsis
• Ferroptosis in rheumatoid arthritis
• Ferroptosis and cardiovascular disease
• Ferroptosis and inflammatory pathways
• Ferroptosis in neurodegenerative diseases
• Lipid metabolism and mediators of inflammation
• Anti-inflammatory and ferroptosis inhibitors
• Ferroptosis-related genes and inflammation