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We observed a consecutive upregulation of molecules associated with inflammation in MI animals throughout the 300-min follow-up period, with strong upregulation of osteopontin, periostin and c-reactive protein (Fig

It also prevents damage to RGCs by scavenging free radicals [15]

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However, as the injury becomes chronic, persistent exposure to immunomodulatory signalsincluding IL-10, TGF-, oxidized phosphatidylethanolamines (oxPEs), and lipid aldehydes like 4-HNEprogressively skews macrophages toward a profibrotic M2-like phenotype (106)