Iron is a pre-requisite for life. As a transition metal, iron has the ability to readily accept and donate electrons, making it both essential and detrimental. Over the past decade, seminal work in this field has demonstrated that free iron initiates a cascade of events that include oxidative stress, leading to tubular damage and activation of immune cells.
Interestingly, it was also recently described that iron-dependent regulated cell death, namely ferroptosis, potentiates kidney injury. In this connection, quenching free iron using chelators such as deferoxamine has led to marked protection against kidney injury.
On the contrary, studies also demonstrate that delivery of iron (or iron-loaded macrophages) to the kidney reduces the severity of the disease. Both of these studies represent our incomplete understanding of the role of iron metabolism in kidney health and pathology.
We invite investigators to contribute original research articles as well as review articles that will aid in the understanding of iron metabolism and trafficking in the initiation and outcomes of kidney injury and chronic kidney disease.
Potential topics include, but are not limited to:
• Characterization and determination of the role of the kidney in iron trafficking and metabolism
• Effects of disorders of systemic iron metabolism (e.g. iron deficiency and iron overload) on the kidney, including new techniques to measure iron content (free or protein-bound) in tissue, plasma and cells
- Iron homeostasis in kidney disease (proteinuria, glomerulopathy and chronic kidney disease)
• Mechanism of iron-mediated kidney injury;
• Modulation of iron and hepcidin levels as therapeutic strategies to overcome injury and/or promote recovery
Iron is a pre-requisite for life. As a transition metal, iron has the ability to readily accept and donate electrons, making it both essential and detrimental. Over the past decade, seminal work in this field has demonstrated that free iron initiates a cascade of events that include oxidative stress, leading to tubular damage and activation of immune cells.
Interestingly, it was also recently described that iron-dependent regulated cell death, namely ferroptosis, potentiates kidney injury. In this connection, quenching free iron using chelators such as deferoxamine has led to marked protection against kidney injury.
On the contrary, studies also demonstrate that delivery of iron (or iron-loaded macrophages) to the kidney reduces the severity of the disease. Both of these studies represent our incomplete understanding of the role of iron metabolism in kidney health and pathology.
We invite investigators to contribute original research articles as well as review articles that will aid in the understanding of iron metabolism and trafficking in the initiation and outcomes of kidney injury and chronic kidney disease.
Potential topics include, but are not limited to:
• Characterization and determination of the role of the kidney in iron trafficking and metabolism
• Effects of disorders of systemic iron metabolism (e.g. iron deficiency and iron overload) on the kidney, including new techniques to measure iron content (free or protein-bound) in tissue, plasma and cells
- Iron homeostasis in kidney disease (proteinuria, glomerulopathy and chronic kidney disease)
• Mechanism of iron-mediated kidney injury;
• Modulation of iron and hepcidin levels as therapeutic strategies to overcome injury and/or promote recovery
