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Auf zellulrer Ebene hat eine In-vitro-Studie von Chang et al

Through the ROS-induced ROS-release (RIRR) mechanism, increased ion flux in membrane channels can further cause the collapse of the mitochondrial membrane potential and the release of ROS [140]

Fine A, McIntosh WB

Under low-density growth conditions, however, the E-cadherinNF2LAST1/2 axis is suppressed, allowing unphosphorylated YAP/TAZ to translocate into the nucleus, upregulating ferroptosis-related genes (e.g., ACSL4, TfR, NADPH oxidase (NOX)1/NOX2/NOX4) and increasing the accumulation of free fatty acids and ROS, ultimately inducing ferroptosis (Wu et al

The mechanism of action of FOXO4-DRI lies in its ability to competitively interfere with the binding of endogenous FOXO4 to the p53 proteina central regulator of the cell cycle and apoptosis