Palmitate drives mitochondrial and ER stress through disruption of the CD73-Adenosine axis

The mGF were treated with BSA control, palmitate, IL-1β, or palmitate plus IL-1β. Gene ontology analysis demonstrated enrichment of pathways related to innate immune activation, oxidative stress, mitochondrial dysfunction, ER stress, and purine metabolism.

Palmitate disrupts the Cd73-adenosine axis while promoting mitochondrial dysfunction, oxidative stress, and Perk-mediated ER stress in gingival fibroblasts. Adenosine signaling protects against lipotoxic-induced ER stress, highlighting the relevance of the Cd73-adenosine pathway for metabolic and inflammatory diseases.