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Building upon these features, we engineered a GshF construct that could be utilized to modulate compartmentalized GSH levels (Fig

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The second coprimary endpoint of change in body weight from baseline was 15.2% vs

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FSP1 reduces exogenous CoQ10 to its hydroquinone form (CoQ10H2), which subsequently eliminates lipid peroxides to suppress ferroptosis and ultimately alleviate intestinal ischemia-reperfusion (I/R) injury, establishing the FSP1/CoQ10 axis as a defined molecular mechanism against ferroptosis