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Moreover, E-cadherin-mediated intercellular interactions downregulate TFRC and ACSL4, reducing ferroptosis sensitivity via the cadherin-Merlin-Hippo-YAP signaling pathway

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Collectively, these studies support the concept that the antioxidant ability of selenoproteins is necessary to mitigate the pro-inflammatory effects of 15-HPETE and reduce endothelial cell death as a consequence of oxidative stress