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The pathophysiology of SCD is complex, involving endothelial activation, BBB disruption, and altered cerebral blood flow dynamics, all driven by chronic inflammation, oxidative stress, and recurrent vaso-occlusive events [195, 196]
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The occurrence of ferroptosis in mature erythrocytes has not been confirmed and it seems quite challenging, since ferroptosis studies suffer from the lack of well-established markers and evaluation of this cell death requires a complex approach with identification of typical cellular and subcellular morphological alterations, genetic hallmarks, biochemical changes, expression of certain ferroptosis-related proteins, etc
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