Cellular Senescence describes an irreversible state of cell cycle arrest adopted by cells in response to accumulated damage, telomere shortening, or chronic proliferative stress. These senescent cells remain metabolically active but lose their ability to divide, often secreting pro-inflammatory molecules. Accumulation of these cells is a significant contributor to tissue aging and chronic disease pathology.
Origin
The term merges ‘cellular,’ referring to the basic unit of life, with ‘senescence,’ meaning the state of being old. It precisely defines the aging process occurring at the microscopic level.
Mechanism
The mechanism involves the activation of tumor suppressor pathways, such as p53 and p16/Rb, which enforce the cell cycle block. Furthermore, the development of the Senescence-Associated Secretory Phenotype (SASP) allows these cells to locally disrupt tissue homeostasis through paracrine signaling.
Using unregulated peptides risks trading short-term goals for long-term biological disarray by introducing unknown variables into your body's delicate hormonal conversation.
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