Lowering either protein worsened aging signs in lab-grown mouse cells
Lowering either protein in lab-grown mouse heart muscle cells increased senescence, a state in which cells stop dividing.
Limit: Senescence marks cells stopping division, rather than measuring heart muscle function
Edited by Boris Djordjevic · AgingResearch.News
Researchers mapped 6,650 proteins across five heart regions in male C57BL/6J mice aged 3, 12 and 20 months, using five mice per age group. They identified two proteins with consistent age-related changes: FTL1 increased, while SERPINA3K decreased.
In experiments using HL-1 mouse heart muscle cells grown in the lab, reducing FTL1 triggered ferroptosis, an iron-dependent form of cell death, and senescence, when cells stop dividing. A drug that inhibits ferroptosis reduced these effects. Reducing SERPINA3K also worsened senescence, while increasing it reduced senescence. In a separate animal experiment, researchers used a virus to increase SERPINA3K specifically in heart muscle cells of 12-month-old mice. Six weeks later, these mice had less heart scarring than mice given a virus without the added gene.
Why it matters
Age-related declines in heart function contribute to cardiovascular disease. The authors identified these proteins as potential targets for interventions against age-related cardiovascular disorders.
Caveats
The mechanistic experiments used a mouse cell line, and the animal work used only males. These findings do not establish benefits in people.
The paper
Multi-region proteomic mapping identifies FTL1 and SERPINA3K as protective factors in cardiac aging
Jinan University
Cell Death & Disease, May 23, 2026, Open access
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