Abstract
A strong mechanistic link between the regulation of iron homeostasis and oxygen sensing is evident in the lung, where both systems must be properly controlled to maintain lung function. Imbalances in pulmonary iron homeostasis are frequently associated with respiratory diseases, such as chronic obstructive pulmonary disease and with lung cancer. However, the underlying mechanisms causing alterations in iron levels and the involvement of iron in the development of lung disorders are incompletely understood. Here, we review current knowledge about the regulation of pulmonary iron homeostasis, its functional importance, and the link between dysregulated iron levels and lung diseases. Gaining greater knowledge on how iron contributes to the pathogenesis of these diseases holds promise for future iron-related therapeutic strategies.
Highlights
Every cell requires sufficient oxygen to satisfy its demand for oxidative metabolism
This review focuses on the regulation of pulmonary iron levels and its functional importance as well as potential intrinsic and extrinsic factors modulating lung iron homeostasis
Cystic Fibrosis (CF) is a severe genetic pulmonary disorder triggered by impaired function of the anion transporter CF transmembrane conductance regulator (CFTR) that results in increased secretion of abnormally viscous mucus and at the clinical level, CF is characterized by chronic bacterial airway infection (e.g., Pseudomonas aeruginosa), prominent neutrophilic inflammation, mucus accumulation within the airways, and progressive bronchiectasis
Summary
Every cell requires sufficient oxygen to satisfy its demand for oxidative metabolism. Red blood cells (RBCs) are in the center of this process by transporting oxygen from the lungs to every tissue. Iron’s critical role is explained by its potential to fluctuate between oxidation states, mainly between divalent ferrous (Fe2+) and trivalent ferric (Fe3+) iron [3] This chemical property as a transition metal makes free iron very reactive and potentially toxic. Iron catalyzes the production of reactive oxygen species (ROS) via the Fenton and Haber-Weiss reactions [4] Exposure to these highly reactive radicals damages lipids, nucleic acids, and proteins, causing cell and tissue damage. This review focuses on the regulation of pulmonary iron levels and its functional importance as well as potential intrinsic and extrinsic factors modulating lung iron homeostasis.
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