Genetic knockout of the farnesoid X receptor (FXR) dramatically shortened both lifespan and healthspan in male mice, accompanied by accelerated neurodegeneration, motor dysfunction, and multi-organ deterioration. Transcriptomic analysis revealed suppressed p53 and PI3K-Akt signaling pathways alongside disrupted bile acid and lipid metabolism in FXR-deficient animals. This finding positions FXR as a master regulator linking bile acid homeostasis to systemic aging processes. The bile acid-longevity connection represents an emerging frontier, as FXR serves as the primary sensor for bile acids that influence everything from gut microbiome composition to metabolic health. Unlike many aging studies focused on caloric restriction or single pathways, this work demonstrates how a nuclear receptor governing metabolic homeostasis can orchestrate lifespan at the organism level. The practical implications are significant given that FXR is druggable, with existing agonists already in clinical development for metabolic diseases. However, the study's limitation to male mice and lack of mechanistic intervention data means clinical translation remains speculative. This represents confirmatory evidence for FXR's role in aging, building on previous correlational studies but providing the first direct genetic proof.