Daniel K. Nomura

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: Overexpression of MAGL in nonaggressive cancer cells recapitulates this fatty acid network and increases their pathogenicity-phenotypes that are reversed by an MAGL inhibitor, indicating that exogenous sources of fatty acids can contribute to malignancy in cancers lacking MAGL activity.

TL;DR: These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.

TL;DR: Individual endocannabinoids generate distinct analgesic profiles that are either sustained or transitory and associated with agonism and functional antagonism of the brain cannabinoid system, respectively.

TL;DR: It is shown that microglia sense SFAs and orchestrate an inflammatory process in the MBH that alters neuronal function when SFA consumption is high, and in this context, microglial depletion enhances leptin signaling and reduces food intake.