Cellular aging, or senescence, is the irreversible process where somatic cells cease to divide and proliferate, yet remain metabolically active, accumulating characteristic functional and structural changes over time. This fundamental biological process is driven by factors such as telomere shortening, DNA damage accumulation, and mitochondrial dysfunction. The presence of senescent cells contributes significantly to chronic inflammation and tissue dysfunction, underpinning many age-related declines in human physiology, including the endocrine system.
Origin
The concept of cellular senescence was first formally described by Leonard Hayflick in the early 1960s, observing that human cells have a finite capacity to replicate, now known as the Hayflick limit. This discovery shifted the focus of aging research from a purely systemic view to one rooted in molecular and cellular biology.
Mechanism
The mechanism of cellular aging is multifaceted, involving the activation of cell cycle arrest pathways, often triggered by irreparable DNA damage or oxidative stress. Senescent cells then acquire a Senescence-Associated Secretory Phenotype (SASP), releasing pro-inflammatory cytokines, chemokines, and proteases into the local tissue microenvironment. This persistent inflammatory signaling disrupts tissue repair and regeneration, contributing directly to age-related pathologies and endocrine system dysregulation.
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