Senescent cells: to eliminate them or silence their inflammation

The accumulation of senescent cells with age is a pivotal mechanism of degenerative aging. Though representing less than 1% of cells in a tissue, their inflammatory signaling disrupts healthy cell behavior and damages tissue structure. The scientific community has developed two complementary strategies: senolytics, which destroy dysfunctional cells, and senomorphic agents, which inhibit their pro-inflammatory signaling pathways (NF-κB, mTOR, JAK/STAT) without eliminating them. Senomorphic drugs allow continuous use and potentially preserve certain physiological functions of senescent cells, while senolytics act intermittently but may leave problematic cells unremoved. The unresolved central dilemma is whether controlled modulation proves superior to selective elimination, especially in contexts like advanced atherosclerosis where senescent cells contribute to structural tissue stability. An integrated strategy adapted to disease stage could be the pathway toward more precise aging therapies.