Leslie Magtanong

TL;DR: AFerroptosis suppressor protein 1 (FSP1) is identified as a key component of a non-mitochondrial CoQ antioxidant system that acts in parallel to the canonical glutathione-based GPX4 pathway, and pharmacological inhibition of FSP1 may provide an effective strategy to sensitize cancer cells to ferroPTosis-inducing chemotherapeutic agents.

TL;DR: It is found that exogenous monounsaturated fatty acids (MUFAs) potently inhibit the non-apoptotic, iron-dependent, oxidative cell death process of ferroptosis and protects cells from apoptotic lipotoxicity caused by the accumulation of saturated fatty acids, but in an ACSL3-independent manner.

TL;DR: It is found that stabilization of wild-type p53 delays the onset of ferroptosis in response to cystine deprivation and is associated with both slower depletion of intracellular glutathione and a reduced accumulation of toxic lipid-reactive oxygen species (ROS).

TL;DR: The roles of lipids in the initiation and execution of necroptosis and other forms of non-apoptotic cell death are reviewed and new technologies allowing for the roles oflipids and lipid metabolism in RCD to be probed in increasingly sophisticated ways are considered.

TL;DR: Glutathione efflux is pinpointed as an unanticipated regulator of ferroptosis sensitivity, due in part to concomitant NRF2-mediated upregulation of MRP1.