Molecule In Gas

Dysregulation of iron metabolism in brain following TBI can result in the accumulation of redoxactive ferrous iron in various brain cells.This is possibly due to alterations in the expressionfunction of regulatory proteins such as ferroportin and ferritin, which fail to export iron from cells and thereby increase the labile iron pool.Although ferritin plays a vital role in iron metabolism by storing excess cellular iron, its precise function in the brain and whether it involves melatonins neuroprotection remain unexplored.It is noted that autophagy is activated to degrade ferritin, which is mediated by the cargo receptor NCOA, thereby increasing iron levels and Targetmol’s Digoxigenin leading to oxidative injury.The fate of excess iron in the absence of ferritin H in astrocytes and microglia remains elusive.Lipid peroxidation is regarded as the driving force of ferroptosis.Although the role of ferroptosis in the pathophysiological process of TBI has been illustrated, future research is required to investigate whether ferroptosis could serve as an intervention target for TBI.Considering distinct mechanisms of ferroptosis inhibition exist, the action of its inhibitors appear to act through different mechanisms.The characterization of new inhibitors should be accompanied by an evaluation of ironchelating or antioxidant activity.For example, melatonin exhibits antioxidant activity, which is probably based on their ability to inhibit ferroptosis.Thus, our findings underscore the protective role of melatonin in inhibiting ferroptosis, supporting the notion that melatonin is an excellent inhibitor of ferroptosis.In conclusion, we report that melatonin produces cerebroprotection in a mouse TBI model, via inhibiting neurological outcome in wildtype mice.Third, loss of neuronal ferritin increases the susceptibility to ferroptosis via an increase in lipid ROS and iron metabolism dysfunction following TBI.The present study sheds new light on the understanding of the diverse biological functions of melatonin, and provides a path for investigating the antiferroptosis actions of melatonin following TBI.Considering the antiferroptosis potential of melatonin, it could be a potential therapeutic target for treating TBI.AUTHOR CONTRIBUTIONS CL, LT, FW, and TR designed the experiments.TR, HW, QL, YC, YG, XM, GC, CG, CW, ZG, SS, JZ, ZW, TW, MZ and CL performed the research.XC, JM, LT, FW and CL provided intellectual contributions throughout the project.FW, XF and JZ contributed essential reagents or tools.CL and TR wrote the manuscript.All authors have read and approved the final manuscript.Estimating the global incidence of traumatic brain injury.Balancing acts: molecular control of mammalian iron metabolism.Systemic and cerebral iron homeostasis in ferritin knockout mice.Conditional deletion of ferritin H in mice induces loss of iron storage and liver damage.Shortterm effects of melatonin and pinealectomy on serotonergic neuronal activity across the lightdark cycle.Melatonin ameliorates neural function by promoting endogenous neurogenesis through the MT melatonin receptor in ischemicstroke mice.Regulation of ferroptotic cancer cell death by GPX.Ablation of ferroptosis regulator glutathione peroxidase in forebrain neurons promotes cognitive impairment and neurodegeneration.Preferential formation of MTMT melatonin receptor heterodimers with distinct ligand interaction properties compared with MT homodimers.The presence and role of iron in mild traumatic brain injury: an imaging perspective.Ferroptosis is an autophagic cell death process.Acute phase response after fatal traumatic brain injury.Mice were sacrificed at the indicated time points after TBI.

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