Abstract
The severity and prevalence Post-Acute COVID-19 Sequela (PACS) or Long-COVID Syndrome (Long- COVID) should not be a surprise. All Long-COVID symptoms may be explained by Oxidative Stress and Parasympathetic and Sympathetic (P&S) dysfunction. This is a retrospective, hypothesis generating, outcomes study.
Highlights
IntroductionJ Neurosci NeuropsycFerroptosis is an iron-dependent and oxidative damage-related form of regulated cell death, which is morphologically, biochemically, and genetically different from other forms of cell death [1]
J Neurosci NeuropsycFerroptosis is an iron-dependent and oxidative damage-related form of regulated cell death, which is morphologically, biochemically, and genetically different from other forms of cell death [1]
We conclude that (1) in contrast to cancer cells, erastin-induced ferroptosis in hippocampal HT22 neurons, despite reduced nuclear receptor coactivator 4 (NCOA4)-levels, (2) that either NCOA4-mediated ferritinophagy does not occur or is of secondary importance in this model, (3) that ferroptosis seems to share some features of the autophagic cell death process
Summary
J Neurosci NeuropsycFerroptosis is an iron-dependent and oxidative damage-related form of regulated cell death, which is morphologically, biochemically, and genetically different from other forms of cell death [1]. It has been reported that cellular iron overload leads to increased reactive oxygen species (ROS) and accumulation of lipid peroxidation in many cell types [2,3,4]. Cells must actively regulate their iron-carrier proteins such as transferrin, lactotransferrin [12]. Cells must buffer their intracellular iron by using cytosolic iron storage proteins such as NCOA4 and ferritins. Mitochondrial ferritin (mtFt) and H-chain ferritin (FTH) are the most known iron storage proteins in the brain. Previous studies suggested that overexpression of mtFt may prevent cytosolic iron accumulation and protect neuroblastoma cells from oxidative stress [18,19]. Mouse brain deficient in ferritin exhibited increased evidence of oxidative stress [22] and oligodendrocytes provide antioxidant functions for neurons by secreting ferritin [23]. It has been reported that ferritinophagy is involved in ferroptosis and that the genetic deletion of NCOA4 inhibits ferritinophagy and blocks lipid peroxidation and ferroptosis by decreasing the levels of bioavailable intracellular iron [12]
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