Interventions aimed at mitigating or reversing cellular senescence, the irreversible arrest of cell division that contributes to aging and age-related pathologies. In the context of hormonal health, these strategies seek to preserve the functional capacity of endocrine tissues and maintain youthful signaling profiles. We focus on reducing the burden of senescent cells that secrete detrimental pro-inflammatory factors, known as the Senescence-Associated Secretory Phenotype (SASP).
Origin
The term originates from the Greek ‘anti’ (against) and ‘senex’ (old man), reflecting a direct opposition to the biological processes of aging. In clinical science, it has gained traction alongside research into cellular hallmarks of aging, particularly those impacting endocrine gland function and tissue turnover. These strategies represent a forward-looking approach to longevity science applied to physiological maintenance.
Mechanism
Key mechanisms include the clearance of senescent cells via senolytics or senomorphics, which modulate their survival or detrimental secretions. Furthermore, optimizing telomere maintenance and enhancing DNA repair pathways are crucial components of this strategy. Supporting robust mitochondrial function also plays a role, as oxidative stress is a major driver of cellular aging within hormone-producing tissues.
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