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doi: 10.1104/pp.108.133777 23 LiableM.BoonrodK

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)

Improvement measures: Neutralizing agents can be combined to eliminate the interference of antibacterial components, or membrane filtration can be adopted to enhance sensitivity

The expression of NOX4, ACSL4 and levels of ROS and iron are increased in the spinal cord of rats subjected to spared nerve injury, while the expression of GPX4 is decreased

In the harsh, inflammatory environment of a fresh wound, many healing cells die off before they can finish their job