SASP and Cellular Senescence: Why Aging Cells Still Send Powerful Signals
Senescent cells do not simply stop dividing. Through SASP signaling, they can reshape local tissue environments, recruit immune activity, influence repair, and contribute to chronic inflammatory research models.
Cellular senescence is often described as a state where cells stop dividing. That is accurate, but incomplete. In modern longevity research, senescent cells are not viewed as silent leftovers. They are metabolically active cells that can change the behavior of their surroundings through a broad secretory program known as the senescence-associated secretory phenotype, or SASP.
The SASP is one reason cellular senescence has become such an important research topic. A senescent cell may no longer proliferate, but it can still release cytokines, chemokines, growth factors, matrix-remodeling enzymes, extracellular vesicle cargo, and other signals that influence nearby cells, immune surveillance, tissue remodeling, fibrosis models, and chronic inflammatory environments.