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ACSL4 plays a dual role in MM: it promotes tumor growth by activating lipid synthesis, but also initiates ferroptosis by catalyzing the production of PUFA-CoA, a key substrate for lipid peroxidation (Zhang et al., 2023)

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We found that cell viability was significantly restored by ferroptosis inhibitor ferrostatin-1 (Fer-1) treatment in ACTL6A-ablated cells but not by apoptosis inhibitor ZVAD-FMK or necroptosis inhibitor necrostatin-1 treatment (Fig

NO production and endothelial NOS expression are decreased in SHR compared with WKY 111,112,113

9b) [204]

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