Systemic Senescence Mechanism describes the overarching biological processes by which cellular aging, characterized by irreversible growth arrest and the secretion of pro-inflammatory factors, propagates throughout the body, ultimately driving organ and system dysfunction. This mechanism involves the accumulation of senescent cells in various tissues, leading to chronic low-grade inflammation, known as the Senescence-Associated Secretory Phenotype (SASP), which actively disrupts the function of neighboring healthy cells. In the hormonal context, this process directly impairs glandular function and reduces target tissue responsiveness. It is a fundamental driver of age-related endocrine decline.
Origin
This term combines ‘systemic’ (affecting the entire body) with ‘senescence mechanism’ (the process of biological aging and decay). It is a core concept in geroscience, moving the focus from individual cell death to the detrimental effects of persistent, metabolically active senescent cells on the entire organism. The concept is a crucial target for anti-aging and longevity research.
Mechanism
The core mechanism involves the accumulation of DNA damage and telomere shortening, triggering a permanent cell cycle arrest. Critically, these senescent cells secrete a complex mixture of cytokines, chemokines, and proteases (SASP) that induce a state of chronic, sterile inflammation throughout the body. This persistent inflammatory milieu impairs the function of the hypothalamic-pituitary axes, reduces hormone receptor sensitivity, and accelerates tissue deterioration, creating a positive feedback loop that promotes further aging and endocrine dysregulation.
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