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in T cells, it modulates Th1/Th2 and Treg/Th17 balance

Critically, these events were most prevalent during initiation/escalation of therapy and declined substantially over time

Existing literature suggests it acts almost like an emergency systemic signal, rushing to stabilize damaged tissue regardless of where the injury is

To date, no classical ferroptosis inhibitors have entered neurodegenerative diseasespecific clinical trials but several antioxidant and radical-trapping agents (RTAs) have/are being evaluated in AD or MCI, including vitamin E (NCT00235716: 2000 IU/d of alpha tocopherol compared with placebo resulted in slower functional decline ~19% delay in clinical progression per year [58]

peptide-handling references consistently flag heat and freezethaw cycling as the main degradation culprits

Histamine and gut mucosal immune regulation