Longevity & AgingCircadian Clock Gene BMAL1 Drives Thyroid Aging by Triggering Cellular Senescence
Researchers used single-cell RNA sequencing of 134,360 human thyroid cells across young, middle-aged, and elderly donors to map aging-related gene changes. They found that aging progressively amplifies cellular senescence—especially in a distinct epithelial subpopulation called CDKN1A_EPI—and that the core circadian clock gene BMAL1 drops significantly with age. Using thyroid-specific Bmal1 knockout mice and cell line experiments, the team showed that loss of BMAL1 suppresses the NF-κB inhibitor NFKBIA, unleashing inflammatory signaling that accelerates senescence and impairs thyroid hormone synthesis. The findings position the BMAL1–NFKBIA axis as a central driver of age-related thyroid dysfunction.
