- Highlights
- Salk scientists identify two cellular programs linked to age-related dysfunction, ferroptosis and senescence, are mechanistically linked through the enzyme acid ceramidase
- The team finds that senescent “zombie” cells are more vulnerable to regulated cell death through ferroptosis and that they can pass that sensitivity on to neighboring cells
- The observations suggest acid ceramidase could be a powerful therapeutic target for supporting healthy aging and preventing age-related diseases and disorders such as arthritis, dementia, and cancer
LA JOLLA—Our population is aging. The United Nations reports that by 2050, the number of people over the age of 85 on our planet is set to triple. But a longer life span isn’t the same as a longer healthspan (the number of years we spend healthy). Salk Institute scientists are working to change that through foundational research that explores the cellular mechanisms driving age-related dysfunction.
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