Role of Iron Dysregulation in Chronic Inflammatory Diseases and Their Complications

Dear Colleagues,

Iron is involved in numerous fundamental biological processes, as it readily switches between ferrous (2+) and ferric (3+) states in electron–transfer reactions. The hepcidin–ferroportin pathway also links cellular iron transport to the regulation of innate immunity and the inflammatory response. Tight compartmentalization and a steady but regulated supply of iron are needed to preserve mitochondrial function, limit oxidative stress, and maintain the health of vital organs. The 2012 characterization of ferroptosis—a regulated form of iron-dependent cell death driven by lipid peroxidation—led to an explosion of research focused on iron and ferroptosis in disease. Altered ferroptosis causes pathological cell loss, inflammation, and tissue fibrosis and is implicated in neurodegeneration, cancer, cardiovascular, renal, and lung diseases, as well as complications of HIV and COVID-19. In metabolically demanding tissues like the brain and heart, inflammation-mediated functional iron deficiency due to poor iron bioavailability (despite adequate or excess tissue iron) may promote organ remodeling and/or dysfunction. The understanding of organ-specific iron handling, iron–mitochondria interdependence, and the best approaches to studying these processes is rapidly evolving.

For this Special Issue, we are interested in original research articles and disease-focused reviews that highlight the role of altered iron homeostasis in chronic inflammatory human diseases and their complications. Contributions involving in vitro, animal, or human studies that use molecular, “-omics” or epidemiologic methods to study iron dysregulation in any of the pathophysiologic processes or diseases mentioned are of particular interest. Studies investigating regulation or novel markers of ferroptosis are also welcome.

Dr. Asha R. Kallianpur
Guest Editor

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• iron
• oxidative stress
• ferroptosis
• inflammation
• chronic disease
• metabolism
• mitochondrial dysfunction