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Hypothetical model of the role of APOE, HRAS1, and LASS1 interactions. Circulating lipids are cleared by APOE and by HDL, which is aided by LASS1-generated ceramide. Metabolic (lipid) stress induces protective survival and stress responses, which are mediated/modulated by HRAS1 and LASS1. Lipotoxicity enhances LASS1 production of ceramide, which signals apoptosis removing damaged cells. These mechanisms become overwhelmed with age resulting in dysfunction and morbidity.
