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The second model featured the intravesicle injection of LPS in the mice (the test group received LPS + beta-caryophyllene through the intravesicle route)

Since GSH is produced in the cytosol but is also required by the mitochondria, we assessed GSH levels in both the cytosol (Cyt) and mitochondria (Mit) following ES-Cu treatment

(33) demonstrated that TRPM4 channels promote oxidized LDL-induced dysfunction specifically in human coronary artery endothelial cells through mechanisms involving ferroptosis

Further, we found NRF2 to be dispensable to the liver upon GSH depletion

Inflammation triggers chondrocyte ferroptosis in TMJOA via HIF-1/TFRC