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Immunohistochemistry analysis revealed that Sorafenib treatment significantly reduced the levels of SLC7A11 and Ki67, a proliferation marker, and increased the level of 4-HNE, a marker of ferroptosis, in tumor tissues (Fig

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Other mechanisms that could potentially explain ferric accumulation in PD are increased lactoferrin receptor in neurons and microvessels, increased DMT1 in DAergic neurons, and genetically-determined impaired in iron transport and binding (Mastroberardino et al., 2009

found that syndecan-1 predicts the prognosis of children with septic shock, and SDX may have therapeutic potential for sepsis-associated endothelial dysfunction (126)