Cellular senescence
Cellular senescence is a state of irreversible cell cycle arrest that can be triggered by a variety of stressors. It is a complex biological process that plays a critical role in a wide range of physiological and pathological phenomena, including aging, tissue repair, cancer, and age-related diseases.
Overview[edit | edit source]
Cellular senescence was first described in the 1960s by Leonard Hayflick, who observed that normal human fibroblasts in culture reach a state of irreversible growth arrest after a certain number of cell divisions, a phenomenon now known as the Hayflick limit. Since then, cellular senescence has been observed in many other cell types and organisms, and its role in biology and disease has been extensively studied.
Mechanisms[edit | edit source]
The mechanisms underlying cellular senescence are complex and multifaceted. They involve a variety of cellular processes, including DNA damage response, telomere shortening, epigenetic changes, and protein homeostasis. These processes lead to changes in cell function and phenotype, including growth arrest, resistance to apoptosis, and secretion of pro-inflammatory and tissue-remodeling factors, collectively known as the senescence-associated secretory phenotype (SASP).
Role in Aging and Disease[edit | edit source]
Cellular senescence plays a dual role in aging and disease. On one hand, it is a potent tumor suppressor mechanism, as it prevents the proliferation of damaged cells that could give rise to cancer. On the other hand, the accumulation of senescent cells and the SASP can contribute to aging and age-related diseases, including cardiovascular disease, neurodegenerative diseases, and diabetes. Recent research has focused on developing strategies to selectively eliminate senescent cells or modulate the SASP, with the aim of improving healthspan and treating age-related diseases.
See Also[edit | edit source]
- Aging
- Cancer
- DNA damage (naturally occurring)
- Hayflick limit
- Senescence-associated secretory phenotype
- Telomere
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