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C., Madsen, K., Doyle, J

doi: 10.1084/jem.20101059

In a mouse model of stroke, intracerebroventricular sodium selenate treatment elevates GPX4 levels by activating transcription factors activating enhancer binding protein 2 and specificity protein 1, while also providing protection against excitotoxicity and endoplasmic reticulum stress-induced cell death independent of GPX4 (102)

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Consistently, a complementary strategy showed that in aged mice, where IGF-I levels are decreased, cardiac overexpression of IGF-I significantly improved cardiomyocyte contractile function[283], attenuating oxidative stress-mediated protein damage, normalizing Ca 2+ homeostasis, reversing age-related alterations in the expression of pro-apoptotic proteins, and decreasing the apoptosis rate[284]

, laser parameters and analyte-matrix co-crystal morphology)