Researchers identify metabolic mechanism behind chronic systemic inflammation

The biological clock of aging often manifests as chronic systemic inflammation, a state where the body remains in a persistent, low-grade inflammatory loop. Researchers from Sanford Burnham Prebys and Mayo Clinic have identified a specific metabolic switch that allows aging cells to trigger this process, revealing that the transition to a pro-inflammatory state is not a random failure, but a coordinated metabolic event. The study focuses on senescent cells—cells that have ceased dividing but remain metabolically active. These cells develop a senescence-associated secretory phenotype (SASP), effectively becoming "inflammatory factories" that leak molecules into surrounding tissues. The key to this transformation lies in the mitochondria. The central mechanism is a change in mitochondrial metabolism that leads to an overproduction of acetyl-CoA. This molecule interacts with histones—the proteins that act as spools for DNA. High levels of acetyl-CoA relax the DNA packaging, loosening the structure without altering the genetic sequence itself. This epigenetic shift exposes specific gene clusters responsible for inflammation, making them accessible for transcription.