An acronym standing for Senescence-Associated Secretory Phenotype, which describes the pro-inflammatory and tissue-damaging factors secreted by senescent, or aged, cells that have ceased dividing. This phenotype is characterized by the release of cytokines, chemokines, and proteases that disrupt the local tissue microenvironment and promote chronic, low-grade systemic inflammation, often referred to as inflammaging. SASP is a major driver of age-related pathology and functional decline across multiple organ systems.
Origin
The concept originated in cell biology and geroscience research, where scientists identified that senescent cells, rather than being inert, actively secrete a harmful cocktail of molecules. The discovery of SASP provided a crucial mechanistic link between cellular aging and chronic disease. Understanding and targeting SASP is a central focus of senolytics research and longevity medicine.
Mechanism
The establishment of SASP is triggered by persistent DNA damage and other cellular stressors that lead to cell cycle arrest. The arrested cell activates transcription factors, notably NF-κB and C/EBPβ, which drive the expression of the SASP factors. These secreted molecules then act in a paracrine manner, inducing senescence in neighboring healthy cells and promoting chronic inflammation, which disrupts normal tissue structure and function, thereby accelerating the overall aging process.
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