Abstract
Iron is at the forefront of a number of pivotal biological processes due to its ability to readily accept and donate electrons. However, this property may also catalyze the generation of free radicals with ensuing cellular and tissue toxicity. Accordingly, throughout evolution numerous pathways and proteins have evolved to minimize the potential hazardous effects of iron cations and yet allow for readily available iron cations in a wide variety of fundamental metabolic processes. One of the extensively studied proteins in the context of systemic and cellular iron metabolisms is ferritin. While clinicians utilize serum ferritin to monitor body iron stores and inflammation, it is important to note that the vast majority of ferritin is located intracellularly. Intracellular ferritin is made of two different subunits (heavy and light chain) and plays an imperative role as a safe iron depot. In the past couple of decades our understanding of ferritin biology has remarkably improved. Additionally, a significant body of evidence has emerged describing the significance of the kidney in iron trafficking and homeostasis. Here, we briefly discuss some of the most important findings that relate to the role of iron and ferritin heavy chain in the context of kidney-related diseases and, in particular, vascular calcification, which is a frequent complication of chronic kidney disease.
Highlights
The ability of iron cations to change its valence serves as a unique and central capacity to contribute in multiple biological pathways, yet underscores its potential hazardous effects mainly by participating in Fenton’s reaction [1,2]
The study by Cohen et al elegantly confirmed the light chain predominance of serum ferritin and its relatively low iron cations content, and provided evidence to support its secretion through the non-classical lysosomal secretory pathway [11]
This study examined the release of iron-rich ferritin and demonstrated that such secretion occurs via the multivesicular body-exosome pathway [15]
Summary
The ability of iron cations (the second most abundant element on earth) to change its valence serves as a unique and central capacity to contribute in multiple biological pathways, yet underscores its potential hazardous effects mainly by participating in Fenton’s reaction [1,2]. It is recognized that levels of serum ferritin rise in response to a number of clinical conditions during inflammatory states and injury models, such as AKI [16,17,18] Such elevation in response to inflammatory stimuli and the relatively iron-poor status of serum ferritin resulted in investigations to examine other potential roles in health and disease that were reviewed by Wang and colleagues [19]. In contrast to FtL, the FtH subunit has crucial ferroxidase activity that converts Fe2+ to Fe3+, facilitating its safe storage in the form of mineral ferrihydrite within the inner wall of the sphere [23,24] Such functional properties have led to a significant amount of investigations into this field, leading to the discovery of seminal findings into the role of this superfamily of proteins in physiological processes and injury models [4,6,25,26]. This review is intended to briefly discuss some of the aspects of ferritin in the context of kidney-related diseases and one of its major cardiovascular complications, namely vascular calcification
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