Ferroptosis is a mode of programmed cell death that manages to be both fairly well explored in the broader research community and far less visible than other programmed cell death processes. It was first named and described a decade ago, though of course researchers have long explored aspects of its biochemistry. There is some thought that ferroptosis may be connected to lysosomal dysfunction and accumulation of molecular waste in long-lived cells of the central nervous system, but in general, it isn’t much mentioned in the aging research field. This paper here provides an overview of why ferroptosis might be an interesting area of investigation, particularly in the context of neurodegenerative conditions.
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Life is indeed continuously going through the irreversible and inevitable process of aging. The rate of the aging process depends on various factors and varies individually. These factors include various environmental stimuli including exposure to toxic chemicals, psychological stress whereas suffering from various illnesses especially chronic diseases serve as endogenous triggers. The basic underlying mechanism for all kinds of stresses is now known to be manifested as production of excessive ROS, exhaustion of ROS neutralizing antioxidant enzymes and proteins leading to an imbalance in oxidation and antioxidant processes with subsequent oxidative stress-induced inflammation affecting the cells, tissues, organs, and the whole body.
All these factors lead to conventional cell death either through necrosis, apoptosis, or autophagy. Currently, a newly identified mechanism of iron-dependent regulated cell death called ferroptosis is of special interest for its implication in the pathogenesis of various diseases such as cardiovascular disease, neurological disorders, cancers, and various other age-related disorders. In ferroptosis, cell death occurs neither by conventional apoptosis, necrosis nor by autophagy, rather dysregulated iron in the cell mediates excessive lipid peroxidation of accumulated lethal lipids. It is not surprising to assume its role in aging as previous research has identified some solid cues on the subject.
In this review, we will highlight the factual evidence to support the possible role and implication of ferroptosis in aging in order to declare the need to identify and explore the interventions to prevent excessive ferroptosis leading to accelerated aging and associated liabilities of aging.
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