Aging
Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and an increased risk of death. Currently, there are co-existing theories on the characteristics of ageing, such as the telomere degradation theory, the mitochondrial functional impairment theory, and the oxidative damage theory. It has been found that excess iron has a strong catalytic potential to increase the production of ROS, causing oxidative damage to cells and ultimately leading to cellular senescence. Numerous studies have shown that the loss of mitochondrial iron homeostasis leads to a decrease in mitochondrial function, which in turn leads to aging.
Iron Homeostasis Disorder Caused by Aging
Recent studies have shown that iron homeostasis and ageing are interrelated. Not only do older people suffer from cellular iron accumulation that can lead to a variety of pathologies and tissue degeneration, but they are also negatively affected by anemia due to impaired iron absorption. The free radical theory of ageing suggests that the cause of ageing is the production of ROS at the mitochondrial level, which over time leads to widespread mitochondrial and cellular dysfunction. When Frataxin, a gene related to iron homeostasis, is inadequate in mitochondria, iron accumulates in the mitochondria, causing oxidative stress and mitochondrial dysfunction, ultimately leading to apoptosis or aging.
Age-related changes in iron homeostasis [1].
Iron Accumulation in Mitochondria
Alterations in mitochondrial iron transport mechanisms lead to the accumulation of mitochondrial iron, which results in the decay of structural components of mitochondria. Iron accumulation usually leads to the development of ferroptosis, and the physiological processes of iron metabolism in senescent cells can generally be studied by mitochondrial imaging, iron accumulation assays, and ROS assays.
Iron Accumulation in Nervous System
Iron senescence occurs primarily in the nervous system and is closely associated with excessive iron ion deposition in the brain. There is growing evidence that damage to macromolecular and cellular components due to disruption of cellular redox homeostasis and imbalance of metal homeostasis is partly responsible for brain aging. The detection of ferritin, neuromelanin, transferrin and iron-containing hemoglobin and iron aggregation in neurons and glial cells is an important approach to study iron senescence.
Iron Metabolism Research Using Animal Models of Aging
Delaying aging and reducing the occurrence of aging-related diseases are fundamental to the problem, and disorders of iron metabolism are an important indicator of the aging process. Assaying iron metabolism indicators in common aging models is an important method to study the association between the two, such as yeast, nematode, Drosophila, zebrafish, and rapid aging mouse models.
Maintaining healthy levels of iron in the blood may be key to improving aging and extending life span, and disorders of iron metabolism are an important indicator of the aging process. Protheragen has many years of research experience in the field of iron metabolism studies in cells and individuals and is committed to providing the broadest range of the highest quality tools for aging research. If you are interested in the services we offer, please contact us for more information.
Reference
- Zhang J, et al. Therapeutic potential of iron chelators on osteoporosis and their cellular mechanisms[J]. Biomedicine & Pharmacotherapy, 2021, 137: 111380.